Fengjie Guo

Tianjin Medical University, T’ien-ching-shih, Tianjin Shi, China

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Publications (20)30.33 Total impact

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    ABSTRACT: MALAT1 is a non-coding RNA overexpressed in non-small cell lung cancer (NSCLC). TDP-43 is a ubiquitously expressed, MALAT1-binding protein implicated in cancer development. We hypothesized that MALAT1 expression level is regulated in lung cancer by TDP-43. We analyzed their functions in cultured NSCLC cells. Downregulation of MALAT1 or TDP-43 expression by siRNA not only markedly suppressed NSCLC cell growth, as measured by the MTT assay in vitro cultured NSCLC cells (P<0.05), but also noticeably impaired the migration and invasion of NSCLC cells, as analyzed by the migration and invasion assay. We also confirm that TDP-43 directly bound to MALAT1 RNA by a RNA immunoprecipitation (RIP) assay and by luciferase reporter activity assay. In a RT-PCR assay, silencing TDP-43 expression effectively decreased MALAT1 RNA transcript level. In contrast, TDP-43 overexpression markedly increased MALAT1 transcript level. In summary, these findings demonstrated that MALAT1 expression by regulation of TDP-43 controls cellular growth, migration, and invasion of NSCLCs. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 08/2015; DOI:10.1016/j.bbrc.2015.08.027 · 2.28 Impact Factor
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    Liang Chang · Fengjie Guo · Bingjie Huo · Yalei Lv · Yudong Wang · Wei Liu
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    ABSTRACT: Gastric cancer is one of the most common malignant tumors and one of the leading causes of cancer-related mortality. Recent studies have revealed that there is a difference in microRNA (miR/miRNA) profiles between cancerous and normal tissues. To find a potentially useful prognostic predictor and a promising therapeutic tool for gastric cancer, the present study investigated the expression and clinical significance of the miR-200 family in gastric cancer. The miR-200 family has five members: hsa-miR-200a, hsa-miR-200b, hsa-miR-200c, hsa-miR-141 and hsa-miR-429. In 46 clinical samples of gastric cancer and paired non-cancerous tissues, the present study observed that the expression levels of the miR-200 family in the cancer tissues were significantly lower than those in the non-cancerous tissues (P<0.001). Lower levels of the five family members were associated with histological grade and the presence of an intravascular cancer embolus (P<0.05). The results revealed that the miR-200 family is downregulated in gastric cancer, and that there are significant differences in the expression of the miR-200 family between normal and cancer tissues. The miR-200 family may therefore become a potentially useful prognostic predictor of the aggressiveness of gastric cancer and a possible therapeutic tool in affected patients.
    Oncology letters 03/2015; 9(5). DOI:10.3892/ol.2015.3028 · 0.99 Impact Factor
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    Fengjie Guo · Fang Yu · Jing Wang · Yongwen Li · Ying Li · Zhigang Li · Qinghua Zhou
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    ABSTRACT: A blood-based biomarker assay is a non-invasive way to screen that can identify lung cancer at an earlier stage to improve the clinical outcome. MALAT1 is a broadly expressed, long non-coding RNA in human tissues and is overexpressed in numerous human carcinomas. The potential of MALAT1 in the whole blood of lung cancer was evaluated. In the present study, blood samples of patients with lung cancer and healthy volunteers (controls) were recruited and analyzed by quantitative polymerase chain reaction (qPCR) for MALAT1 expression and clinicopathological data. Lung cancer tissues were also analyzed by qPCR. The expression of MALAT1 in the whole blood of lung cancer was lower compared to the control. The area under the receiver operator curve was 0.718 (P<0.001). Relatively, the expression of MALAT1 was stronger in the whole blood of lung cancer with metastasis compared to non-metastasis. Additionally, the whole blood with bone or brain metastasis exhibited a higher expression of MALAT1 compared to the blood with lymph node or pleura metastasis. Subsequently, a lower expression of MALAT1 was detected in metastatic lymph node tissues than that of the carcinoma in situ of the lung. Taken together, these results indicate that MALAT1 as a biomarker to screen lung cancer may represent a host response to lung cancer.
    02/2015; 3(3). DOI:10.3892/br.2015.422
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    ABSTRACT: Gastric cancer remains a worldwide burden as the second leading cause of cancer-related death. Drug resistance of chemotherapy looms as a major clinical obstacle to successful treatment. Recent evidence indicated that miRNA-200c can restore the sensitivity of NSCLC cells to cisplatin and cetuximab. The expression of miRNA-200c and RhoE were investigated in gastric cancer tissues and cells (SGC7901 and SGC7901/DDP) by qRT-PCR. A luciferase reporter assay was done to understand the potential correlation between miRNA-200c and RhoE. Pre-miR-200c was transfected in SGC7901/DDP cells to confirm whether miRNA-200c could regulate RhoE expression. RhoE was knocked down to explore the role of RhoE on sensitivity of chemotherapy in gastric cancer by MTT. Western blot analysis was performed to further explore the mechanism of RhoE in regulating drug resistance. The results showed that miRNA-200c was significantly lower in cancerous tissues than those in the paired normal tissues, whereas the expression of RhoE was just the opposite. The significant difference of miRNA-200c and RhoE were observed between SGC7901 cells and SGC7901/DDP cells. miRNA-200c has target sites in the 3'-UTR of RhoE mRNA by luciferase reporter assay. Transfection of pre-miR-200c reduces RhoE expression. Meanwhile, the knockdown of RhoE enhanced the sensitivity of SGC7901/DDP cells and changed expression of some genes. These suggested that miRNA-200c regulated the sensitivity of chemotherapy to cisplatin (DDP) in gastric cancer by possibly targeting RhoE.
    Pathology & Oncology Research 07/2013; DOI:10.1007/s12253-013-9664-7 · 1.81 Impact Factor
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    ABSTRACT: STC1 is a glycoprotein hormone involved in calcium/phosphate (Pi) homeostasis. There is mounting evidence that STC1 is tightly associated with the development of cancer. But the function of STC1 in cancer is not fully understood. Here, we found that STC1 is down-regulated in Clinical tissues of cervical cancer compared to the adjacent normal cervical tissues (15 cases). Subsequently, the expression of STC1 was knocked down by RNA interference in cervical cancer CaSki cells and the low expression promoted cell growth, migration and invasion. We also found that STC1 overexpression inhibited cell proliferation and invasion of cervical cancer cells. Moreover, STC1 overexpression sensitized CaSki cells to drugs. Further, we showed that NF-κB p65 protein directly bound to STC1 promoter and activated the expression of STC1 in cervical cancer cells. Thus, these results provided evidence that STC1 inhibited cell proliferation and invasion through NF-κB p65 activation in cervical cancer.
    PLoS ONE 01/2013; 8(1):e53989. DOI:10.1371/journal.pone.0053989 · 3.23 Impact Factor
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    ABSTRACT: The purpose of this study was to investigate the efficacy of Endostar combined with chemotherapy on human esophageal squamous cell carcinoma Eca-109 in mice. The tumor xenograft models were established and randomly assigned to 4 groups: control group, Endostar group (1.5 mg/kg day, once daily for 3 weeks), chemotherapy group (Paclitaxel 10 mg/kg day, Cisplatin 5 mg/kg day, for 1, 7, 14, 21 days), and chemotherapy + Endostar group (combination). The length and width of tumor were measured and the tumor volumes (cm(3)) were calculated every other day. Three weeks later, the mice were executed, and the tumor tissues were collected to weigh and analyse the histopathology and proliferation for tumor xenograft. The results demonstrated that the tumor volumes and weight in chemotherapy + Endostar group were significantly lower than that in other three groups. Meanwhile, the cell proliferation of tumor xenograft in combined treatment group was significantly lower than that in other three groups. It was concluded that Endostar combined with chemotherapy could obviously enhance the inhibitory effect on esophageal squamous cell carcinoma Eca-109 in mice.
    Molecular Biology Reports 10/2012; 40(1). DOI:10.1007/s11033-012-2106-x · 1.96 Impact Factor
  • Fengjie Guo · Yaguang Fan · Youlin Qiao · Qinghua Zhou
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    ABSTRACT: Lung cancer is one of malignant tumors harming human health. Over the past five decades, there is increasing morbidity and mortality of lung cancer which is the leading cause of cancer morbidity and mortality worldwide. Risk factors of lung cancer are versatile and smoking is among the important ones, but there are some non-smoking men, especially for women, some of whom developed lung cancer. Many studies showed that human papillomavirus (HPV) was the risk factor of lung cancer, however, which was less comprehensive or seriously estimated. The results of research on relationship between HPV infection and lung cancer are different because of the difference of detection methods, geographical distribution and sample size. Recently, the relationship of HPV and lung cancer is increasingly thought highly with deep study. Study advance of relationship between HPV and lung cancer in the recent years is briefly reviewed.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 03/2012; 15(3):191-4. DOI:10.3779/j.issn.1009-3419.2012.03.11
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    ABSTRACT: It is important to understand the mechanisms of tumor development for curing cervical cancer. However, the molecular basis determining the different characteristics of tumor remains unclear. Space environment as a special study model can expand the study field of tumor development. To approach this, after human cervical carcinoma CaSki cells were flown on “Shen Zhou IV” space shuttle mission, the cell morphology and proliferation was investigated after flying to ground. We found that the growth of 48A9 CaSki cell (flight group) became slow compared with ground groups. Observation of cells by light microscopy revealed differences in cell morphology between ground controls and flight groups, and the flight group exhibited morphologic differences, characterized by rounder, smoother, decreased, smaller and low-adhension cells. Transmission electron microscope images showed the structure of the ultrastructural characteristics of 48A9 CaSki cells were clearly distinct from those of the ground CaSki cells in aspects of mitochondrion, cytoplasm, nucleus and ribosomes. MTT and soft agar assay showed that 48A9 CaSki cells grew slowly compared to ground control. Furthermore, suppression subtractive hybridization combining with reverse Northern blot was used to identify differently expression genes between flight and ground groups. These differentially expressed genes included cytoskeleton, cell differentiation, cell apoptosis, signal transduction, DNA repair, protein synthesis, substance metabolism, and antigen presentation. The identification of differently expressed genes which is likely to increase our understanding of the molecular processes underlying tumor development will provide new insight into tumor development mechanisms, and may facilitate the development of new anticancer strategies.
    Molecular Biology Reports 02/2012; 39(6):6923-31. DOI:10.1007/s11033-012-1519-x · 1.96 Impact Factor
  • Guangsu Xun · Fengjie Guo · Zhigang Li · Qinghua Zhou
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 10/2011; 14(10):790-800. DOI:10.3779/j.issn.1009-3419.2011.10.05
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    ABSTRACT: To express and purify the human scFv antibody,SA3,against the hepatoma fused to enhanced green fluorescent protein,and to observe the targeted capacity of fusion protein EGFP-SA3 in vivo. SA3 and EGFP genes were cloned into plasmid pET-25b(+) to construct the recombinant plasmid EGFP-SA3/pET-25b(+),followed by DNA sequencing. Then it was transformed into E.coli BL21(DE3) and induced for fusion expression of EGFP-SA3 with IPTG. The expressed fusion protein EGFP-SA3 was purified and detected with SDS-PAGE. HepG2 cells were incubated with the fusion protein EGFP-SA3 in vitro,and the binding bioactivity was observed under the fluorescent microscope. Further more,we injected the EGFP-SA3 by caudal vein into nude mice planted by hepatoma and observed the whole body fluorescence image of EGFP. SA3 and EGFP genes were successfully cloned into pET-25b(+),which was confirmed by restriction enzyme NcoI-XhoI or NcoI-EcoRI. A band migrated at the position 750 bp,same to EGFP gene,emerged when recombinant plasmid was digested by restriction enzyme NcoI-EcoRI. Similarly,a band,about 1 500 bp,emerged when digested by NcoI-XhoI. The open-reading frame was confirmed by DNA sequencing. Fusion protein EGFP-SA3 was expressed as inclusion body. After purification and refolding,the result of immunofluorescence detection verified that EGFP-SA3 could specifically bind to HepG2 cells and maximum tumor penetration was at 24 h after the injection. The purified fusion protein EGFP-SA3 has strong binding capacity to HepG2 cells,indicating the scFv SA3 has a potential value as a targeting molecule for diagnosis and targeted therapy for liver cancer.
    Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 10/2011; 36(10):979-86. DOI:10.3969/j.issn.1672-7347.2011.10.008
  • Jiajia Wang · Yalin Li · Fengjie Guo · Guohua Zhou · Guancheng Li
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    ABSTRACT: To obtain I50 anti-idiotype antibody and identify its activity in vitro. I50 anti-idiotype (Id) antibody gene was amplified from the template of fuse 5-I50 by PCR to construct a prokaryotic expression vector pET25b-I50. The expression of pET25b-I50 in E. coli BL21(DE3) was induced by isopropylthio-β-D-galactopyranoside (IPTG) and was confirmed by SDS-PAGE and Western blot with Ab1(FC2) monoclonal antibody and an anti-hexahistidine tag antibody. The method of dialysis refolding was used to restore the activity of I50 anti-Id antibody, which was measured by Dot-ELISA and lymphocyte proliferation assay. The recombinant vector was successfully constructed and the recombinant protein was successfully expressed and purified with 90% purity. The relative molecular weight of the expressed protein was 15 kD, which was in accordance with expectation. The activity of I50 anti-Id antibody could be restored and could promote the proliferation of lymphocyte in a dose-dependent manner. These results suggested that I50 anti-Id protein vaccine is likely an option in the therapy against nasopharyngeal carcinoma in vivo.
    Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 03/2011; 36(3):185-91. DOI:10.3969/j.issn.1672-7347.2011.03.001
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    ABSTRACT: Artemin (ARTN) is a neurotrophic factor belonging to the glial cell-derived neurotrophic factor family of ligands. To develop potential therapy targeting ARTN, we studied the roles of miR-223 in the migration and invasion of human esophageal carcinoma. ARTN expression levels were detected in esophageal carcinoma cell lines KYSE-150, KYSE-510, EC-9706, TE13, esophageal cancer tissues and paired non-cancerous tissues by Western blot. Artemin siRNA expression vectors were constructed to knockdown of artemin expression mitigated migration and invasiveness in KYSE150 cells. Monolayer wound healing assay and Transwell invasion assay were applied to observe cancer cell migration and invasion. The relative levels of expression were quantified by real-time quantitative PCR. ARTN expression levels were higher in esophageal carcinoma tissue than in the adjacent tissue and was differentially expressed in various esophageal carcinoma cell lines. ARTN mRNA contains a binding site for miR-223 in the 3'UTR. Co-transfection of a mir-223 expression vector with pMIR-ARTN led to the reduced activity of luciferase in a dual-luciferase reporter gene assay, suggesting that ARTN is a target gene of miR-223. Overexpression of miR-223 decreased expression of ARTN in KYSE150 cells while silencing miR-223 increased expression of ARTN in EC9706 cells. Furthermore, overexpression of miR-223 in KYSE150 cells decreased cell migration and invasion. Silencing of miR-223 in EC9706 cells increased cell migration and invasiveness. These results reveal that ARTN, a known tumor metastasis-related gene, is a direct target of miR-223 and that miR-223 may have a tumor suppressor function in esophageal carcinoma and could be used in anticancer therapies.
    Journal of Biomedical Science 03/2011; 18(1):24. DOI:10.1186/1423-0127-18-24 · 2.74 Impact Factor
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    ABSTRACT: To investigate the significance of mammalian target of rapamycin (mTOR) and its active form, p-mTOR in colorectal carcinomas. Immunohistochemistry was used to detect the expression of mTOR and p-mTOR proteins in 108, 40 and 40 tissue samples from colorectal carcinoma, normal colonic mucosa and adenomatous polyps samples, respectively. The correlation of mTOR and p-mTOR expression with clinicopathological characteristics of colorectal carcinoma was analyzed. The positive rates of mTOR and p-mTOR were significantly higher in colorectal carcinoma (61.1% and 61.1%, respectively, p<0.05) than in normal colonic mucosa (7.5% and 2.5%) and adenomatous polyps (27.5% and 20%). Overexpression of total mTOR protein was significantly associated with T1/T2 stage tumors, lymph node metastasis, distal metastasis) and degree of differentiation. p-mTOR overexpression was additionaly linked with degree of differentiation and TNM stage. The overexpression of mTOR and p-mTOR may play important roles in colorectal carcinogenesis with relations to the degree of differentiation, invasiveness and metastasis.
    Asian Pacific journal of cancer prevention: APJCP 01/2011; 12(10):2581-4. · 2.51 Impact Factor
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    ABSTRACT: Tuberculosis (TB) is a disease of worldwide public-health concern. The development of resistance to an increasing number of second-line drugs and those used to treat multidrug-resistant (MDR) TB is rapidly becoming an emergency that could hinder the prevention and treatment of TB globally. This study describes the resistance profile of MDR and extensively drug-resistant (XDR) TB with a hospital-based survey in Beijing, China, conducted in the period 2007 to 2009. Drug-susceptibility tests performed on 967 Mycobacterium tuberculosis strains isolated from 967 patients showed that the rate of resistance to at least one first-line and at least one second-line drug was 70.1% and 60.7%, respectively. The overall MDR rate was 19.4%, and 14.9% of the MDR cases were XDR. In conclusion, MDR and XDR TB represent a significant number of total TB cases, therefore effective measures to manage these resistant strains are desperately needed. Development of a national TB policy in China might be a key method for solving the present problems of TB management.
    09/2010; 63(5):368-71.
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    ABSTRACT: Hepatocellular carcinoma (HCC) is the most common malignancy in the world, especially in China. Early diagnosis of new and recurrent hepatocellular carcinoma, followed by timely treatment, will help decrease mortality. Currently biomarkers are not satisfactory. Better diagnostic methods are highly demanded. In this study, we have used in silico identification and RT-PCR test and discovered a hepatoma associated gene (HTA). Knockdown of endogenous HTA expression was performed by small interfering RNA in malignant hepatocyte HepG2. Then we tested the cell proliferative ability of these cells in vitro and in vivo. HTA was expressed specifically in some kinds of tumors, but not detected in any normal tissues. It was expressed especially high in hepatocellular carcinoma. Knockdown of endogenous HTA expression in HepG2 by small interfering RNA attenuated HCC cell growth. HCA is a very good marker for tumors, especially for HCC. It could play important roles in HCC development and progression and can be a promising molecular target for the development of new diagnostic and therapeutic strategies for HCC.
    Journal of Cancer Research and Clinical Oncology 08/2010; 136(8):1187-92. DOI:10.1007/s00432-010-0767-1 · 3.01 Impact Factor
  • Fengjie Guo · Yalin Li · Yan Liu · Jiajia Wang · Guancheng Li
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    ABSTRACT: Cisplatin has been shown to induce apoptosis in various types of cancer cells. Despite the great efficacy at treating certain kinds of cancers, cisplatin introduced into clinical use shows side effects and the acquisition or presence of resistance to the drug. Thus, it is important that we further understand the anti-cancer mechanism of cisplatin with the goal of enhancing its efficacy. ADP-ribosylation factor-like 6 interacting protein 1 (ARL6IP1) is an apoptotic regulator. We studied cisplatin-induced apoptosis with suppression of ARL6IP1 expression in CaSki cervical cancer cells. Exogenous expression of ARL6IP1 suppressed cisplatin-induced apoptosis in CaSki cells, and siRNA-induced silencing of ARL6IP1 triggered apoptosis in CaSki cells even in the absence of other apoptotic stimuli. Cisplatin treatment induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK expression, and suppressed Bcl-2 and Bcl-xl expression, whereas cells transfected with pcDNA3.1-ARL6IP1 showed lower levels of cisplatin-induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK up-regulation and higher levels of cisplatin-suppressed Bcl-2 and Bcl-xl down-regulation. These novel findings collectively suggest that ARL6IP1 may play a key role in cisplatin-induced apoptosis in CaSki cervical cancer cells by regulating the expression of apoptosis-associated proteins such as caspase-3, -9, p53, NF-kappaB, MAPK, Bcl-2, Bcl-xl, and Bax.
    Oncology Reports 05/2010; 23(5):1449-55. · 2.19 Impact Factor
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    Fengjie Guo · Yalin Li · Yan Liu · Jiajia Wang · Yuehui Li · Guancheng Li
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    ABSTRACT: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is suggested to be a long (∼7 kb) non-coding RNA. MALAT1 is overexpressed in many human carcinomas, but its function remains unknown. To investigate the role of MALAT1 in human cervical cancer progression, we designed and used short hairpin RNA to inhibit MALAT1 expression in CaSki cells and validated its effect on cell proliferation and invasion. Changes in gene expression were analyzed by reverse transcriptase–polymerase chain reaction. Our data demonstrated that MALAT1 was involved in cervical cancer cell growth, cell cycle progression, and invasion through the regulation of gene expression, such as caspase-3, -8, Bax, Bcl-2, and Bcl-xL, suggesting that MALAT1 could have important implications in cervical cancer biology. Our findings illustrate the biological significance of MALAT1 in cervical cancer progression and provide novel evidence that MALAT1 may serve as a therapeutic target in the prevention of human cervical cancer.
    Acta Biochimica et Biophysica Sinica 03/2010; 42(3):224-9. DOI:10.1093/abbs/gmq008 · 2.09 Impact Factor
  • Fengjie Guo · Yan Liu · Yalin Li · Guancheng Li
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    ABSTRACT: ADP-ribosylation factor-like 6 interacting protein 1 (ARL6IP1) is an apoptotic regulator. To investigate the role of ARL6IP1 in human cervical cancer progression, we designed and used short hairpin RNA (shRNA) to inhibit ARL6IP1 expression in CaSki cells and validated its effect on cell proliferation and invasion. Changes in gene expression were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) or western blot. Down-regulation of ARL6IP1 expression by infection with ARL6IP1-specific RNAi-expressing vector inhibited CaSki cell proliferation and colony formation. In addition, down-regulation of ARL6IP1 expression arrested CaSki cell cycling at the G0/G1 phase and mitigated CaSki cell migration, determined by wound healing assays. ARL6IP1 was involved in cervical cancer cell growth, cell cycle progression, and invasion through regulation of gene expression, such as Caspase-3, Caspase-9, p53, TAp63, NF-κB, MAPK, Bcl-2, and Bcl-xL, suggesting that ARL6IP1 could have important implications in cervical cancer biology. Our findings illustrate the biological significance of ARL6IP1 in cervical cancer progression, and provide novel evidence that ARL6IP1 may serve as a therapeutic target in the prevention of human cervical cancer.
    Molecular Biology Reports 03/2010; 37(8):3819-25. DOI:10.1007/s11033-010-0037-y · 1.96 Impact Factor
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    ABSTRACT: The early diagnosis of colorectal cancer (CRC) is important because it is one of the most readily curable of all cancers, if detected early. However, the sensitivity of current markers is low. Immunostaining intensity for the monoclonal antibody Hb3 in CRC cell lines and tissues was stronger than in controls. Interestingly, this was associated with a low level of tumor differentiation. We used Hb3-coupled affinity chromatography to search for a corresponding Hb3 antigen as a candidate biomarker for early detection, and identified a Rho GTPase activating protein 6 (RhoGAP6) isoform 1 variant as an Hb3 antigen by mass spectrometry. Using reverse transcription polymerase chain reaction and western blot analysis, we confirmed that the expression levels of this variant were elevated in aberrant cells and tissues. Thus, the RhoGAP6 isoform 1 variant might serve as a biomarker for the development and progression of CRC.
    Pathology & Oncology Research 12/2009; 16(3):319-26. DOI:10.1007/s12253-009-9226-1 · 1.81 Impact Factor
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    ABSTRACT: The identification of tumor-associated antigens, which are specifically expressed in cancer tissues, is very important for immunotherapy of lung cancer. We have combined the in silico screening and experimental verifying to identify genes that are differently expressed in cancers compared with their corresponding normal tissues. Using these methods, we have identified that GABRA3 gene was overexpressed in lung cancer and rarely expressed in other cancers. Furthermore, GABRA3 protein expression was significantly higher in the lower grade of lung cancer. It may compose functional GABA-gated channel with other subunits. This study demonstrated GABRA3 could be a potential biomarker for diagnosis of lung cancer, and GABAA receptors may play an important role in cancer differentiation.
    Pathology & Oncology Research 01/2009; 15(3):351-8. DOI:10.1007/s12253-008-9128-7 · 1.81 Impact Factor

Publication Stats

165 Citations
30.33 Total Impact Points


  • 2011–2013
    • Tianjin Medical University
      • Department of Radiology
      T’ien-ching-shih, Tianjin Shi, China
  • 2009–2012
    • Central South University
      • • Xiangya Hospital
      • • Cancer Research Institute
      Ch’ang-sha-shih, Hunan, China