Wenjing Sun

Harbin Medical University, Charbin, Heilongjiang Sheng, China

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Publications (35)129.45 Total impact

  • Jie Xu · Peng Liu · Xiangning Meng · Jing Bai · Songbin Fu · Rongwei Guan · Wenjing Sun ·
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    ABSTRACT: Double minute chromosomes (DMs) are the cytogenetic hallmark of extra-chromosomal genomic amplification. They can well represent the advanced stage of malignancy. However, the mechanisms of DM generation are still not fully understood. Here, the sister chromatid exchange (SCE) was used to determine whether the occurrence of DMs was related to the high genomic instability in human carcinoma cells. We analyzed SCE frequencies in two groups of cell lines: the first group contained DM-positive cell lines such as UACC-1598, SK-PN-DW, and NCI-N87 carcinomas, while the second group comprised DM-negative cell lines including HO-8910, U251, and MGC-803. The data showed that SCE was significantly increased in the DM-positive cells as compared to the DM-negative cells. In addition, there was a positive correlation between the incidence of DMs and the SCE frequency in the UACC-1598, SK-PN-DW, and NCI-N87 carcinoma cells. Because SCE can reflect general genome instability, it is suggested that the DMs are likely to be closely associated with genomic instability in carcinoma cells. Meanwhile, SCE may be involved in the malignant progression of DM-positive cancers.
    Molecular Cytogenetics 12/2015; 8(1). DOI:10.1186/s13039-015-0192-x · 2.14 Impact Factor
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    ABSTRACT: We used a panel of 17 non-small-cell lung cancer cell lines to investigate whether the presence of polymorphisms in the RRM1, ERCC1, ABCB1 and MTHFR genes and alterations in their mRNA expression can affect the in vitro chemosensitivity to cisplatin and gemcitabine. Polymorphisms in these genes were evaluated by direct sequencing. mRNA expression levels were assessed by realtime PCR. In vitro chemosensitivity to cisplatin and gemcitabine was expressed as IC50 values, using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay. There was a significant, positive correlation between RRM1 mRNA expression and IC50 values for gemcitabine (r = 0.6533, p = 0.0045), and there was a significant, negative correlation between ABCB1 mRNA expression and IC50 values for cisplatin (r = -0.5459, p = 0.0287). When examining the association between the polymorphisms and IC50, we found that only the MTHFR 1298A>C polymorphism showed a tendency to be more chemosensitive to gemcitabine (p = 0.0440). These in vitro results suggest that mRNA expression levels of the RRM1 and ABCB1 genes may be useful indicators of chemosensitivity to gemcitabine and cisplatin, respectively. The MTHFR 1298A>C polymorphism was associated with gemcitabine chemosensitivity, which require further functional analysis with co-expressed genes and should be explored in prospective clinical studies to determine its potential clinical application as a predictive biomarker. Original submitted 11 February 2014; Revision submitted 3 November 2014.
    Pharmacogenomics 01/2015; 16(1):23-34. DOI:10.2217/pgs.14.159 · 3.22 Impact Factor
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    ABSTRACT: Gene amplification is a frequent manifestation of genomic instability that plays a role in tumour progression and development of drug resistance. It is manifested cytogenetically as extrachromosomal double minutes (DMs) or intrachromosomal homogeneously staining regions (HSRs). To better understand the molecular mechanism by which HSRs and DMs are formed and how they relate to the development of methotrexate (MTX) resistance, we used two model systems of MTX-resistant HT-29 colon cancer cell lines harbouring amplified DHFR primarily in (i) HSRs and (ii) DMs. In DM-containing cells, we found increased expression of non-homologous end joining (NHEJ) proteins. Depletion or inhibition of DNA-PKcs, a key NHEJ protein, caused decreased DHFR amplification, disappearance of DMs, increased formation of micronuclei or nuclear buds, which correlated with the elimination of DHFR, and increased sensitivity to MTX. These findings indicate for the first time that NHEJ plays a specific role in DM formation, and that increased MTX sensitivity of DM-containing cells depleted of DNA-PKcs results from DHFR elimination. Conversely, in HSR-containing cells, we found no significant change in the expression of NHEJ proteins. Depletion of DNA-PKcs had no effect on DHFR amplification and resulted in only a modest increase in sensitivity to MTX. Interestingly, both DM-containing and HSR-containing cells exhibited decreased proliferation upon DNA-PKcs depletion. We demonstrate a novel specific role for NHEJ in the formation of DMs, but not HSRs, in MTX-resistant cells, and that NHEJ may be targeted for the treatment of MTX-resistant colon cancer. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Journal of Medical Genetics 12/2014; 52(2). DOI:10.1136/jmedgenet-2014-102703 · 6.34 Impact Factor
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    ABSTRACT: Gene transcription analysis is important in cancer research, and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) has been demonstrated to be an effective method to evaluate gene transcription in cancer. RT‑qPCR requires an internal reference gene with a consistent level of mRNA transcription across various experimental conditions. However, it has been suggested that different treatments, including anticancer therapy, may influence the transcriptional stability of internal reference genes. Paclitaxel (PTX) and 10‑hydroxycamptothecin (HCPT) are widely used to treat various types of cancer, and a suitable internal reference gene is required in order to analyze the transcription profiles of the cells following treatment. In the current study, the transcriptional stability of 30 candidate reference genes was investigated in cancer cells following treatment with PTX and HCPT. The two ovarian cancer cell lines, UACC‑1598 and SKOV3, were treated with PTX and HCPT for 24 and 48 h, and the transcriptional levels of the candidate reference genes were subsequently evaluated by RT‑qPCR analysis. The transcriptional stability of the selected genes was then analyzed using qbase+ and NormFinder software. A total of 9 genes were demonstrated to exhibit high transcriptional stability and one of these genes, ribosomal protein L13a (RPL13A), was identified to exhibit high transcriptional stability in every group. The current study identified various reference genes suitable under different circumstances, while RPL13A was indicated to be the most suitable reference gene for analyzing the transcription profile of ovarian cancer cells following treatment with PTX and HCPT.
    Molecular Medicine Reports 12/2014; 11(4). DOI:10.3892/mmr.2014.3108 · 1.55 Impact Factor
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    ABSTRACT: Double minute chromosomes (DMs) are extrachromosomal cytogenetic structures found in tumor cells. As hallmarks of gene amplification, DMs often carry oncogenes and drug resistance genes, and play important roles in malignant tumor progression and drug resistance. The mitogen-activated protein kinase (MAPK) signaling pathway is frequently dysregulated in human malignant tumors which induces genomic instability, but it remains unclear whether a close relationship exists between MAPK signaling and DMs. In the present study, we focused on three major components of MAPK signaling, ERK1/2, JNK1/2/3 and p38, to investigate the relationship between MAPK and DM production in tumor cells. We found that the constitutive phosphorylation of ERK1/2, but not JNK1/2/3 and p38, was closely associated with DMs in tumor cells. Inhibition of ERK1/2 activation in DM-containing and ERK1/2 constitutively phosphorylated tumor cells was able to markedly decrease the number of DMs, as well as the degree of amplification and expression of DM-carried genes. The mechanism was found to be an increasing tendency of DM DNA to break, become enveloped into micronuclei (MN) and excluded from the tumor cells during the S/G2 phases of the cell cycle, events that accompanied the reversion of malignant behavior. Our study reveals a linkage between ERK1/2 activation and DM stability in tumor cells.
    The Journal of Pathology 11/2014; 235(1). DOI:10.1002/path.4439 · 7.43 Impact Factor
  • Xianyin Xia · Ruirui Du · Lingbo Zhao · Wenjing Sun · Xiumei Wang ·
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    ABSTRACT: Astrocyte elevated gene-1 (AEG-1) expression is up-regulated in various human cancers and plays an important role in tumorigenesis and progression. The aim of this study was to explore AEG-1 expression in oral squamous-cell carcinoma (OSCC) and to assess whether it is associated with microvessel density (MVD), metastasis, and survival. Specimens from 87 patients with OSCC were investigated by immunohistochemistry staining for AEG-1 and MVD. By statistical analysis, we studied the correlations between the expression of AEG-1 and MVD and various clinicopathologic factors, including overall survival (OS). We found that AEG-1 was highly expressed in 51.72% of OSCC. Expression was closely correlated with differentiation, clinical stage, T classification, and lymph node metastasis. The MVD had similar results. Expression of AEG-1 correlated positively with MVD. The lymph-node metastatic rate in patients with high AEG-1/high MVD was significantly higher than in patients with high AEG-1/low MVD, low AEG-1/high MVD, or low AEG-1/low MVD. Patients with high AEG-1 expression showed far lower OS rates than those with low expression. For MVD, there were similar results. Only AEG-1 and MVD expression were independent prognostic factors for OS by multivariate analysis. Expression of AEG-1 may be correlated with tumor angiogenesis and metastasis and is a valuable prognostic factor in patients with OSCC.
    Human pathology 04/2014; 45(4). DOI:10.1016/j.humpath.2013.08.030 · 2.77 Impact Factor
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    Zehua Bian · Yang Yu · Terigele Yang · Chao Quan · Wenjing Sun · Songbin Fu ·
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    ABSTRACT: Single-base substitution may affect the function of genes. This study identified a single-base substitution of G for A in codon 148 of cyclin-dependent kinase inhibitor 2A (CDKN2A/p16) by sequencing human ovarian cancer cell line UACC-1598. As a tumor suppressor gene, the expression of CDKN2A/p16 should be strictly controlled. In order to control CDKN2A/p16 gene expression, an inducible pTUNE vector system was selected. Using recombinant DNA technology, a CDKN2A/p16-A148T and CDKN2A/p16-wild-type gene expression system was successfully constructed to investigate whether this single-base substitution affects the function of CDKN2A/p16. For the wild-type and the mutant, expression of CDKN2A/p16-green fluorescent protein fusion protein increased markedly following isopropyl-β-D-thiogalactoside induction, and was accompanied by significant G1 arrest in the transfected human ovarian cancer SKOV3 cell line. The inducible vectors used in this study, CDKN2A/p16-wild-type and CDKN2A/p16-A148T open reading frame, may be useful for further investigation into whether this somatic mutation could alter the function of CDKN2A/p16 as a tumor suppressor gene. In summary, CDKN2A/p16-A148T was identified in ovarian cancer cells, and this single-base substitution did not affect the ability of CDKN2A/p16 to arrest the cell cycle.
    Oncology letters 04/2014; 7(4):1229-1232. DOI:10.3892/ol.2014.1867 · 1.55 Impact Factor
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    ABSTRACT: Double minute chromosomes (DMs) are a hallmark of gene amplification. The relationship between the formation of DMs and the amplification of DM-carried genes remains to be clarified. The human colorectal cancer cell line NCI-H716 and human malignant primitive neuroectodermal tumor cell line SK-PN-DW are known to contain many DMs. To examine the amplification of DM-carried genes in tumor cells, we performed Affymetrix SNP Array 6.0 analyses and verified the regions of amplification in NCI-H716 and SK-PN-DW tumor cells. We identified the amplification regions and the DM-carried genes that were amplified and overexpressed in tumor cells. Using RNA interference, we downregulated seven DM-carried genes, (NDUFB9, MTSS1, NSMCE2, TRIB1, FAM84B, MYC, and FGFR2) individually and then investigated the formation of DMs, the amplification of the DM-carried genes, DNA damage, and the physiological function of these genes. We found that suppressing the expression of DM-carried genes led to a decrease in the number of DMs and reduced the amplification of the DM-carried genes through the micronuclei (MN) expulsion of DMs from the tumor cells. We further detected an increase in the number of γH2AX foci in the knockdown cells, which provides a strong link between DNA damage and the loss of DMs. In addition, the loss of DMs and the reduced amplification and expression of the DM-carried genes resulted in a decrease in cell proliferation and invasion ability. © 2013 Wiley Periodicals, Inc.
    International Journal of Cancer 03/2014; 134(6). DOI:10.1002/ijc.28467 · 5.09 Impact Factor
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    ABSTRACT: Gene amplifications in the 17q chromosomal region are observed frequently in breast cancers. An integrative bioinformatics analysis of this region nominated the MAP3K3 gene as a potential therapeutic target in breast cancer. This gene encodes mitogen-activated protein kinase kinase kinase 3 (MAP3K3/MEKK3), which has not yet been reported to be associated with cancer-causing genetic aberrations. We found that MAP3K3 was amplified in approximately 8-20% of breast cancers. Knockdown of MAP3K3 expression significantly inhibited cell proliferation and colony formation in MAP3K3-amplified breast cancer cell lines MCF-7 and MDA-MB-361 but not in MAP3K3 non-amplified breast cancer cells. Knockdown of MAP3K3 expression in MAP3K3-amplified breast cancer cells sensitized breast cancer cells to apoptotic induction by TNFα and TRAIL, as well as doxorubicin, VP-16 and fluorouracil, three commonly used chemotherapeutic drugs for treating breast cancer. In addition, ectopic expression of MAP3K3, in collaboration with Ras, induced colony formation in both primary mouse embryonic fibroblasts and immortalized human breast epithelial cells (MCF-10A). Combined, these results suggest that MAP3K3 contributes to breast carcinogenesis and may endow resistance of breast cancer cells to cytotoxic chemotherapy. Therefore, MAP3K3 may be a valuable therapeutic target in patients with MAP3K3-amplified breast cancers, and blocking MAP3K3 kinase activity with a small molecule inhibitor may sensitize MAP3K3-amplified breast cancer cells to chemotherapy.
    The Journal of Pathology 01/2014; 232(1). DOI:10.1002/path.4283 · 7.43 Impact Factor
  • Lingbo Zhao · Yang Yu · Jie Wu · Jing Bai · Yuzhen Zhao · Chunming Li · Wenjing Sun · Xiumei Wang ·
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    ABSTRACT: Oral squamous cell carcinoma (OSCC) is a common human malignancy with high incidence rate and poor prognosis. Although the polycomb group protein enhancer of zeste homolog 2 (EZH2) plays a crucial role in cell proliferation and differentiation during the occurring and development progress of several kinds of malignant tumors, the impact of EZH2 on the development and progression of OSCC is unclear. In this study, we demonstrate that EZH2 is overexpressed in OSCC cells and clinical tissue. With in vitro RNAi analysis, we generated stable EZH2 knocking down cell lines from two OSCC cell lines, with two sh-RNAs targeting to EZH2, respectively. We found that knocking down of EZH2 could decrease the proliferation ability and induce apoptosis of OSCC cells. Moreover, we demonstrated that of EZH2 inhibition decreased the migration and metastasis of OSCC cells. In conclusion, the results of the current study demonstrated an association between EZH2 expression and OSCC cell development. We recommend that EZH2 acts as an oncogene and plays an important role in OSCC carcinogenesis.
    Gene 01/2014; 537(2). DOI:10.1016/j.gene.2014.01.006 · 2.14 Impact Factor
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    ABSTRACT: Congenital cataract is a Mendelian disorder that frequently causes blindness in infants. To date, various cataract-associated loci have been mapped; more than 30 genes have been identified by linkage analysis. However, the pathogenic loci in some affected families are still unknown, and new research strategies are needed. In this study, we used linkage-exome combinational analysis to further investigate the pedigree of a four-generation Chinese family with autosomal dominant coralliform cataract. We combined whole exome sequencing and linkage analysis to identify the causative mutation. The exome capture and next-generation sequencing were used to sequence the protein-coding regions in the genome of the proband to identify rare mutations, which were further screened for candidate mutations in linkage regions. Candidate mutations were independently verified for co-segregation in the whole pedigree using Sanger sequencing. We identified a C to A transversion at nucleotide position c.70 in exon 2 of CRYGD, a cataract-associated gene. This mutation resulted in a threonine substitution for proline at amino acid residue 24. We identified a missense P24T mutation in CRYGD that was responsible for coralliform cataract in our studied family. Our findings suggest that the combination of exome sequencing and linkage analysis is a powerful tool for identifying Mendelian disease mutations that might be missed by the classic linkage analysis strategy.
    BMC Medical Genetics 10/2013; 14(1):107. DOI:10.1186/1471-2350-14-107 · 2.08 Impact Factor
  • Xianyin Xia · Zhaozhao Man · Hui Jin · Ruirui Du · Wenjing Sun · Xiumei Wang ·
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    ABSTRACT: Purpose: To investigate the effect of Vitapex on the healing of periapical lesions and the expression of bone morphogenetic protein (BMP-2) during the periapical bone regeneration. Materials and methods: Periapical lesions were induced in Sprague-Dawley (S-D) rats by an occlusal pulp exposure in the mandibular first molars and were verified by X-ray. Total of 36 rats were randomly divided into three groups, and they were obturated with Zinc Oxide Eugenol (ZOE), or with Vitapex, or non-treated as negative control group. The rats of three groups were randomly killed at week 0, 2, 4, and 8 after root canal therapy, and then the mandibles were processed for histological examination and immunohistochemistry analysis. Results: At week 0, only a few BMP-2 positive cells could be observed in all rats. While the expression of BMP-2 was dramatically increased in case of Vitapex group at week 2 and week 4, and then climaxed at week 8. However, no apparent changes were observed in ZOE group and negative group at week 2, 4, and 8. Conclusion: These observations suggested that Vitapex has a greater ability in inducing bone regeneration than ZOE by the expression of BMP-2 induction in the treatment of rats experimental periapical lesions.
    Journal of Indian Society of Pedodontics and Preventive Dentistry 10/2013; 31(4):249-253. DOI:10.4103/0970-4388.121825
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    ABSTRACT: Double minute chromosomes are cytogenetic manifestations of gene amplification frequently seen in cancer cells. Genes amplified on double minute chromosomes include oncogenes and multi-drug resistant genes. These genes encode proteins which contribute to cancer formation, cancer progression, and development of resistance to drugs used in cancer treatment. Elimination of double minute chromosomes, and therefore genes amplified on them, is an effective way to decrease the malignancy of cancer cells. We investigated the effectiveness of a cancer drug, gemcitabine, on the loss of double minute chromosomes from the ovarian cancer cell line UACC-1598. Gemcitabine is able to decrease the number of double minute chromosomes in cells at a 7500X lower concentration than the commonly used cancer drug hydroxyurea. Amplified genes present on the double minute chromosomes are decreased at the DNA level upon gemcitabine treatment. Gemcitabine, even at a low nanomolar concentration, is able to cause DNA damage. The selective incorporation of double minutes chromatin and γ-H2AX signals into micronuclei provides a strong link between DNA damage and the loss of double minute chromosomes from gemcitabine treated cells. Cells treated with gemcitabine also showed decreased cell growth, colony formation, and invasion. Together, our results suggest that gemcitabine is effective in decreasing double minute chromosomes and this affects the biology of ovarian cancer cells.
    PLoS ONE 08/2013; 8(8):e71988. DOI:10.1371/journal.pone.0071988 · 3.23 Impact Factor
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    ABSTRACT: Double minutes (DMs) are hallmarks of gene amplification. However, their molecular structure and the mechanisms of formation are largely unknown. To elucidate the structure and underlying molecular mechanism of DMs, we obtained and cloned DMs using micro-dissection and degenerated oligonucleotide primed PCR (DOP-PCR) from the ovarian cancer cell line UACC-1598. Two large amplicons, the 284 Kb AmpMYCN, originating from locus 2p24.3, and the 391 Kb AmpEIF5A2, from locus 3q26.2, were found co-amplified on the same DMs. The two amplicons are joined through a complex 7 Kb junction DNA sequence. Analysis of the junction has revealed three de novo created small palindromes surrounding the six breakpoints. Consistent with these observations, we further found that 70% of the 57 reported DM junction sequences have de novo creation of small palindromic sequences surrounding the breakpoints. Together, our findings indicate that de novo-generated small palindromic sequences are characteristic of amplicon boundary junctions on DMs. It is possible that the de novo-generated small palindromic sequences, which may be generated through non-homologous end joining in concert with a novel DNA repair machinery, play a common role in amplicon rejoining and gene amplification.
    International Journal of Cancer 08/2013; 133(4). DOI:10.1002/ijc.28084 · 5.09 Impact Factor
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    ABSTRACT: Toll-like receptors (TLRs) and the nuclear factor-kappa B (NF-κB) signaling transduction pathway play important roles in the pathogenesis of several chronic inflammatory diseases, but its function in oral lichen planus (OLP) remains unclear. In this study, we examined the expression of TLR4 and NF-κB-p65 and inflammatory cytokines TNF-α and IL-1β by immunohistochemistry in OLP tissues, and found that TLR4 and NF-κB-p65 were significantly upregulated in OLP compared to normal oral mucosa (P<0.05). We used keratinocytes HaCaT stimulated with lipopolysaccharide (LPS) to simulate the local OLP immune environment to some extent. RT-PCR and immunoblotting analyses showed significant activation of TLR4 and NF-κB-p65 in the circumstance of LPS-induced inflammatory response. The high expression of TLR4 and NF-κB-p65 are correlated with expression of cytokines TNF-α and IL-1β (P<0.05). We further showed that NF-κB could act as an anti-apoptotic molecule in OLP. We conclude that TLR4 and the NF-κB signaling pathway may interact with the perpetuation of OLP. Steroids and cyclosporine are effective in the treatment of symptomatic OLP. However, there was some weak evidence for the mechanism over Dexamethasone (DeX) and Cyclosporine A (CsA) for the palliation of symptomatic OLP. In the present study, we found that Dexamethasone and Cyclosporine A negatively regulated NF-κB signaling pathway under LPS simulation in HaCaT cells by inhibiting TLR4 expression, on the other hand, Cyclosporine A could inhibit HaCaT cell proliferation by the induction of the apoptosis of HaCaT cells to protect OLP from the destruction of epidermal cells effectively.
    Gene 08/2012; 508(2):157-64. DOI:10.1016/j.gene.2012.07.045 · 2.14 Impact Factor
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    ABSTRACT: The production of type I interferon must be tightly regulated and aberrant production of type I interferon is harmful or even fatal to the host. TBK1 phosphorylation at Ser172 plays an essential role in TBK1-mediated antiviral response. However, how TBK1 activity is negatively regulated remains poorly understood. Using a functional genomics approach, we have identified PPM1B as a TBK1 phosphatase. PPM1B dephosphorylates TBK1 in vivo and in vitro. PPM1B wild-type but not its phosphatase-deficient R179G mutant inhibits TBK1-mediated antiviral response and facilitates VSV replication in the cells. Viral infection induces association of PPM1B with TBK1 in a transient fashion in the cells. Conversely, suppression of PPM1B expression enhances virus-induced IRF3 phosphorylation and IFNβ production. Our study identifies a previously unrecognized role for PPM1B in the negative regulation of antiviral response by acting as a TBK1 phosphatase.
    Cellular Signalling 06/2012; 24(11):2197-204. DOI:10.1016/j.cellsig.2012.06.017 · 4.32 Impact Factor
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    ABSTRACT: Human non-small cell lung cancer (NSCLC) is one of the most common malignancies in the modern world. Its recurrence is mainly due to its ability to invade and metastasize. However, the precise mechanism for tumor development and metastasis is still not fully understood. To shed light on the development of lung cancer, the human giant cell lung carcinoma cell lines 95D with high metastatic potential and 95C with low metastatic potential were selected in this study. The 2 cell lines originated from the same parental cell and share a similar genetic background. In the current study, we identified 3 differentially expressed proteins in 95C and 95D cell lines, namely, PAI-RBP1, C1orf142, and COTL1, by using 2-dimensional electrophoresis proteomics analysis. We found that PAI-RBP1 and C1orf142 expression levels were higher in 95D than in 95C cells, whereas COTL1 expression level was lower in 95D when compared to 95C cells. We also confirmed these results by reverse transcription-polymerase chain reaction and immunoblotting analyses. The messenger RNA and protein levels of PAI-RBP1 and C1orf142 were much higher in 95D than in 95C cells, and COTL1 expression level was lower in 95D than in 95C cells. The PAI-RBP1 expression was assessed by immunohistochemistry in 70 NSCLC and 7 normal lung tissue samples from patients. PAI-RBP1 expression level was higher in tumor tissues (positive staining in 87.1% of cases [61/70]) than in normal tissues (positive staining in 14.3% of cases [1/7]). In conclusion, by studying protein expression in NSCLC cell lines with high and low metastasis as well as in human lung cancer tissues, we have identified 3 proteins, namely, PAI-RBP1, C1orf142, and COTL1, which were differentially expressed in NSCLC cell lines with different metastatic potential. In addition, we also found that PAI-RBP1 might contribute to NSCLC development.
    Journal of Investigative Medicine 02/2012; 60(4):689-94. · 1.69 Impact Factor
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    ABSTRACT: A meta-analysis and systematic review assessing randomised controlled trials (RCTs) was sought to determine whether subcutaneous injection of insulin with hypertonic glucose promotes healing in postoperative incisions with aseptic fat liquefaction. We searched the Cochrane library, Pubmed, EMBASE, National Science Digital Library (NSDL) and China Biological Medicine Database (CBMdisc) for literature published from 1 January 1990 to 30 September 2011. RCTs that evaluated subcutaneous injection of insulin with hypertonic glucose as a treatment for postoperative wound with fat liquefaction were sought. Wound healing was the primary endpoint. Jadad score and Cochrane Collaboration's tool were used for assessing quality of studies and risk of bias. We abstracted data regarding time to wound healing, cost and adverse effects. The random-effects inverse variance model was used for all analyses using weighted mean difference and 95% confidence interval. Eight trials (414 participants) were identified that met the inclusion criteria. Subcutaneous injection of insulin with hypertonic glucose significantly reduces time to healing by 6·33 days compared with conventional drainage, with less cost. There was no report concerning adverse effects. Subcutaneous injection of insulin with hypertonic glucose may improve the healing process in postoperative wounds with aseptic fat liquefaction.
    International Wound Journal 02/2012; 10(1). DOI:10.1111/j.1742-481X.2012.00949.x · 2.15 Impact Factor
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    ABSTRACT: The adenosine triphosphate (ATP)-binding cassette, sub-family B, member 1 (ABCB1) gene encodes P-glycoprotein (Pgp), which plays an important role in drug disposition by limiting intracellular uptake of paclitaxel. ABCB1 gene polymorphisms may alter the expression and function of Pgp, thereby influencing the response to chemotherapy. A panel of 17 non-small cell lung cancer (NSCLC) cell lines was used to investigate whether alterations in the ABCB1 gene or its mRNA expression correlated with in vitro chemosensitivity to paclitaxel. Polymorphisms in the ABCB1 gene were evaluated by direct sequencing. mRNA expression levels were assessed by quantitative real-time reverse transcription PCR. In vitro chemosensitivity to paclitaxel was expressed as half-maximal inhibitory concentration values, using a tetrazolium (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide)-based colorimetric assay. The variant allele frequencies for four ABCB1 gene polymorphisms were 14.71% for 2677G>T/A, 32.35% for 2734T>C, 23.53% for 3396C>T and 76.47% for 3435C>T. There was a significant positive correlation between ABCB1 mRNA expression and half-maximal inhibitory concentration values for paclitaxel (r=0.5322, P=0.0279). None of the four ABCB1 gene polymorphisms were associated with paclitaxel chemosensitivity or ABCB1 mRNA expression in the 17 cell lines. These in vitro results suggest that high ABCB1 mRNA expression may be a predictive biomarker for poor chemosensitivity to paclitaxel. The panel of NSCLC cell lines may provide clues and indications for establishing clinically useful relationships between a given polymorphism or level of gene expression and chemosensitivity to an anti-cancer agent.
    Respirology 08/2011; 16(8):1228-34. DOI:10.1111/j.1440-1843.2011.02050.x · 3.35 Impact Factor
  • Xiumei Wang · Wenjing Sun · Chengren Zhang · Guohua Ji · Yana Ge · Ye Xu · Yuzhen Zhao ·
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    ABSTRACT: Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine that regulates cell growth, differentiation, migration, apoptosis and extracellular matrix remodeling. TGF-β1 transduces signals from the cell membrane to the cell nucleus through serine/threonine kinase receptors and their downstream effectors, Smad molecules. Although many studies have been focused on TGF-β1-Smad signaling pathway, the role of TGF-β1/Smad in tongue squamous cell carcinoma is not fully understood. In the present study, we used a series of cell function assays to examine the role of TGF-β-Smad4 signaling in tongue squamous cell carcinoma. We observed the effects of TGF-β1 on the growth and metastatic potential of the tongue squamous cell carcinoma cell line Ts, which expresses lower level of Smad4 protein. We found that Smad4 could decrease TGF-β1-induced cell proliferation, and that Smad4 overexpression promoted Ts cell apoptosis. In Ts vector control cells, TGF-β1 increased the expression of TβRII, as well as MMP-2, and enhanced cell invasion through the basement membrane, and then induced cell metastasis. However in Ts cells stably expressing Smad4, Smad4 mediated TGF-β1-induced p21 expression promoted cell apoptosis and inhibited cell proliferation, delayed MMP-2 expression, and decreased cell metastasis. Therefore, TGF-β1 plays distinct roles in the Smad4-dependent and -independent signaling pathways.
    Gene 06/2011; 485(2):160-6. DOI:10.1016/j.gene.2011.06.023 · 2.14 Impact Factor

Publication Stats

371 Citations
129.45 Total Impact Points


  • 2008-2015
    • Harbin Medical University
      • Laboratory of Medical Genetics
      Charbin, Heilongjiang Sheng, China
  • 2008-2014
    • Baylor College of Medicine
      • Department of Pediatrics
      Houston, Texas, United States
  • 2013
    • Government of the People's Republic of China
      Peping, Beijing, China