Guihua Wang

Tongji Hospital, Wu-han-shih, Hubei, China

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Publications (16)46.43 Total impact

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    ABSTRACT: Imatinib is the first-line drug for gastrointestinal stromal tumors (GISTs), as mutated KIT is closely associated with the occurrence of GIST. However, Imatinib resistance (IMA-resistance) occurs inevitably in most GIST patients. Although the over-expression of KIT in GIST is one of the major factors contributing to IMA-resistance, the underlying mechanism is still unclear. In this study, we demonstrate that p55PIK, an isoform of phosphoinositide 3-kinase (PI3K), increases KIT expression, leading to IMA-resistance in GISTs by activating NF-κB signaling pathway. Furthermore, down-regulation of p55PIK significantly decreases KIT expression and re-sensitizes IMA-resistance-GIST cells to Imatinib in vitro and in vivo. Interestingly, the expression of both p55PIK and KIT proteins is significantly increased in tumor samples from IMA-resistance-GIST patients, suggesting that p55PIK up-regulation may be important for IMA-resistance in the clinical setting. Altogether, our data provide evidence that p55PIK-PI3K signaling can contribute to IMA-resistance in GIST by increasing KIT expression. Moreover, p55PIK may be a novel potential drug target for treating tumors that develop IMA-resistance.
    Oncotarget 11/2015; DOI:10.18632/oncotarget.6011 · 6.36 Impact Factor
  • Feng Lv · Yang Yu · Guihua Wang · Junbo Hu · Bin Zhang · Wei You · Jing Wang ·
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    ABSTRACT: To understand the association between the cytokine network and psoriasis, the present study cultured human keratinocytes (HaCaT cells) and investigated the effects of the phosphatidylinositol‑3‑kinase (PI3K) p55 regulatory subunit (p55PIK), and its N‑terminal 24 amino acids (N24) on the regulation of endotoxin (LPS)‑induced cytokine secretion. The results of the enzyme‑linked immunosorbent assay and reverse transcription quantitative polymerase chain reaction revealed an increased release of the inflammatory cytokines, tumor necrosis factor (TNF)‑α, interleukin (IL)‑6 and IL‑8 in the HaCaT cells following LPS stimulation. Transfection with the adenovirus (AD)‑N24‑green fluorescent protein (GFP) suppressed the release of these cytokines, whereas AD‑p55PIK‑GFP increased their release. Immunocytochemistry detected a low level of nuclear factor (NF)‑κB p65 staining in quiescent HaCaT cells, which was localized primarily in the cytoplasm. LPS stimulation induced the translocation of NF‑κB p65 protein into the nucleus and intense staining suggested increased expression. Transfection with AD‑N24‑GFP reduced the expression of NF‑κB p65 in the nucleus. Western blot analysis demonstrated that AD‑N24‑GFP downregulated the expression levels of the Toll‑like receptor (TLR)2/TLR4/myeloid differentiation factor 88 (MyD88) pathway components in the HaCaT cells, without affecting the PI3K/Akt signaling pathway. Transfection with AD‑p55PIK‑GFP resulted in an increased expression level of MyD88 protein and phosphorylated Akt. Co‑transfection with AD‑N24‑GFP and AD‑p55PIK‑GFP did not significantly alter the levels of phosphorylated extracellular‑signal‑regulated kinases 1/2, c‑Jun N‑terminal kinases or p38, indicating that AD‑N24‑GFP and AD‑p55PIK‑GFP did not affect the mitogen‑activated protein kinase signaling pathway. In conclusion, AD‑N24‑GFP effectively inhibited the LPS‑induced expression levels of TNF‑α, IL‑6 and IL‑8. The elevated expression of p55PIK synergized with LPS and promoted the release of inflammatory cytokines. AD‑N24‑GFP and AD‑p55PIK‑GFP affected LPS‑induced inflammatory cytokine release in the HaCaT cells through the TLRs/MyD88 signaling pathways.
    Molecular Medicine Reports 01/2015; 11(5). DOI:10.3892/mmr.2015.3184 · 1.55 Impact Factor
  • Guihua Wang · Xi Yang · Yuan Jin · Yu Deng · Xuelai Luo · Junbo Hu · Jing Wang ·
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    ABSTRACT: PIK3R3, an isoform of class IA phosphoinositide 3-kinase (PI3K), specifically interacts with cell proliferation regulators, such as retinoblastoma and proliferation cell nuclear antigen, to promote cell proliferation. However, the mechanisms behind the upstream signaling pathway of PIK3R3 remain unclear to date. This study showed that PIK3R3 expression was regulated by transforming growth factor-β (TGF-β) signaling and that PIK3R3 mediated the TGF-β-induced inhibition of lung adenocarcinoma cell proliferation. TGF-β down-regulated PIK3R3 expression in lung adenocarcinoma cells. However, this TGF-β-induced inhibition of cell proliferation can be attenuated by PIK3R3 overexpression. In addition, TGF-β can attenuate the transcriptional activity of NKX2.1, a transcription factor that binds to the promoter of PIK3R3. This result indicated that TGF-β regulated PIK3R3 expression by targeting NKX2.1. We confirmed the correlation between NKX2.1 and PIK3R3 in clinical samples. Therefore, the TGF-β/NKX2.1/PIK3R3 axis is crucial in the TGF-β-induced inhibition of cell proliferation, and the NKX2.1/PIK3R3 axis might become a target in TGF-β receptor-repressed lung adenocarcinoma. © 2014 Wiley Periodicals, Inc.
    Molecular Carcinogenesis 11/2014; 54(S1). DOI:10.1002/mc.22243 · 4.81 Impact Factor
  • Guihua Wang · Xi Yang · Chuan Li · Xiaonian Cao · Xuelai Luo · Junbo Hu ·
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    ABSTRACT: Class IA phosphatidylinositol 3-kinase (PI3K) plays an essential role in the invasion and metastasis of cancer. However, the mechanisms and specific functions of PI3K isoforms in tumor invasion and metastasis are not fully understood. We evaluated the role of PIK3R3, a PI3K regulatory subunit encoded by the PIK3R3 gene, in colorectal cancer (CRC) invasion and metastasis. Clinic specimens and cell lines data shows the expression level of PIK3R3 is associated with CRC metastasis. Over-expression of PIK3R3 increases tumor migration and invasion in vitro, and promotes metastasis of CRCs in vivo. Furthermore, we investigates that over-expression of PIK3R3 depend on SNAI2 inducing significant epithelial-to-mesenchymal transition (EMT). Down-regulation of PIK3R3 reverses this process, which possibly contributes to the enhanced invasive and metastasizing abilities of CRC cells. In this study, we found that PIK3R3 plays an important role in CRC metastasis, and might be a potential and specific target for therapies against metastatic CRC.
    Molecular Cancer Therapeutics 05/2014; 13(7). DOI:10.1158/1535-7163.MCT-14-0049 · 5.68 Impact Factor
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    ABSTRACT: Previously, we demonstrated that p55PIK, an isoform of Class IA phosphatidylinositol 3 kinase (PI3K), specifically interacts with important cell cycle regulators such as Rb to promote cell cycle progression. Here, we used GST-pull down assay to identify other p55PIK-interacting proteins besides Rb in a Rb-deficient cell line and found that p55PIK interacted with proliferation cell nuclear antigen (PCNA), which plays a key role in co-ordinating both initiation of the leading strand DNA replication and discontinuous lagging strand synthesis. Over-expression of p55PIK increased, and knockdown decreased, DNA synthesis and DNA replication by modulating the binding of DNA polymerase δ (Polδ) to PCNA. Moreover, a cell-permeable peptide containing the N-terminal binding domain of p55PIK (TAT-N24) disrupted p55PIK-PCNA interaction in cancer cells, and also inhibited DNA synthesis and tumor growth in cell culture and in vivo. Altogether, our results show that p55PIK-PCNA interaction is important in regulating DNA synthesis and contributes to tumorigenesis. Furthermore, p55PIK-PCNA interaction provides a potential new target for anti-cancer drug development.
    Molecular Cancer Therapeutics 08/2013; 12(10). DOI:10.1158/1535-7163.MCT-12-0920 · 5.68 Impact Factor
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    Yu Deng · Jing Wang · Guihua Wang · Yuan Jin · Xuelai Luo · Xianmin Xia · Jianping Gong · Junbo Hu ·
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    ABSTRACT: p55PIK, regulatory subunit of class IA phosphatidylinositol 3-kinase (PI3K), plays a crucial role in cell cycle progression by interaction with tumor repressor retinoblastoma (Rb) protein. A recent study showed that Rb protein can localize to the mitochondria in proliferative cells. Aberrant p55PIK expression may contribute to mitochondrial dysfunction in cancer progression. To reveal the mechanisms of p55PIK transcriptional regulation, the p55PIK promoter characteristics were analyzed. The data show that myeloid zinc finger 1, MZF1, is necessary for p55PIK gene transcription activation. ChIP (Chromatin immuno-precipitation) assay shows that MZF1 binds to the cis-element "TGGGGA" in p55PIK promoter. In MZF1 overexpressed cells, the promoter activity, expression of p55PIK, and cell proliferation rate were observed to be significantly enhanced. Whereas in MZF1-silenced cells, the promoter activity and expression of p55PIK and cell proliferation level was statistically decreased. In CRC tissues, MZF1 and p55PIK mRNA expression were increased (P = 0.046, P = 0.047, resp.). A strong positive correlation (Rs = 0.94) between MZF1 and p55PIK mRNA expression was observed. Taken together, we concluded that p55PIK is transcriptionally activated by MZF1, resulting in increased proliferation of colorectal cancer cells.
    03/2013; 2013:868131. DOI:10.1155/2013/868131
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    ABSTRACT: Vascular growth factor (VEGF) is an important mediator of angiogenesis. PI3K plays essential roles in angiogenesis; however, the mechanisms and specific functions of individual isoforms of PI3K members in tumor angiogenesis regulation are still not fully understood. In this study, we evaluate the role of p55PIK, a PI3K regulatory subunit encoded by PIK3R3 gene, in tumor angiogenesis. We reported that overexpression of p55PIK in cancer cells up-regulated HIF-1α expression and increased VEGF expression. Furthermore, overexpression of p55PIK increased tumor angiogenesis in vivo and in vitro. Moreover, data indicated enhanced HIF-1α expression by p55PIK-PI3K depended on its ability to activate NF-кB signaling pathways, especially to increase the phosphorylation of p65 subunits of NF-κB. Our study suggested that p55PIK-PI3K was essential in regulating cancer cell-mediated angiogenesis and contributed to tumor growth and that the p55PIK provides a potential and specific target for new anti-angiogenesis drug development.
    Angiogenesis 01/2013; 16(3). DOI:10.1007/s10456-013-9336-y · 4.88 Impact Factor
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    ABSTRACT: Angiogenesis plays a pivotal role in tumor growth. The hypoxia- inducible factor 1, α subunit (HIF-1α)/vascular endothelial growth factor pathway is the most important pathway for regulating angiogenesis in the tumor microenvironment. c-Myc is an important oncogene that has many biological functions. In this study, we investigated the role of c-Myc in tumor angiogenesis. We found that the overexpression of c-Myc in colon cancer cells could promote the expression of HIF-1α and that of vascular endothelial growth factor. Moreover, we found that c-Myc regulated HIF-1α at the post-transcriptional level. The results revealed c-Myc-dependent regulation of HIF-1α instead of HIF-1α-dependent c-Myc regulation for the first time. They also showed that c-Myc was essential to regulate colon cancer cell-mediated angiogenesis and contributed to tumor growth. This research provides the theoretical basis for clinical trials of new therapeutic targets of c-Myc and HIF-1α in colon cancer cells.
    Biochemical and Biophysical Research Communications 12/2012; 430(2). DOI:10.1016/j.bbrc.2012.12.006 · 2.30 Impact Factor
  • Senyan Lai · Guihua Wang · Xiaonian Cao · Zhaoming Li · Junbo Hu · Jing Wang ·
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    ABSTRACT: This study examined the role of EMP-1 in tumorigenesis of non-small cell lung carcinoma (NSCLC) and the possible mechanism. Specimens were collected from 28 patients with benign lung diseases and 28 with NSCLC, and immunohistochemically detected to evaluate the correlation of EMP-1 expression to the clinical features of NSCLC. Recombinant adenovirus was constructed to over-express EMP-1 and then infect PC9 cells. Cell proliferation was measured by Ki67 staining. Western blotting was performed to examine the effect of EMP-1 on the PI3K/AKT signaling. Moreover, tumor xenografts were established by subcutaneous injection of PC9 cell suspension (about 5×10(7)/mL in 100 μL of PBS) into the right hind limbs of athymic nude mice. The results showed EMP-1 was significantly up-regulated in NSCLC patients as compared with those with benign lung diseases. Over-expression of EMP-1 promoted proliferation of PC9 cells, which coincided with the activation of the PI3K/AKT pathway. EMP-1 promoted the growth of xenografts of PC9 cells in athymic nude mice. It was concluded that EMP-1 expression may contribute to the development and progress of NSCLC by activating PI3K/AKT pathway.
    Journal of Huazhong University of Science and Technology 12/2012; 32(6):834-8. DOI:10.1007/s11596-012-1043-1 · 0.83 Impact Factor
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    ABSTRACT: While there is strong evidence for phosphatidylinositol 3-kinase (PI3K) involvement in cancer development, there is limited information about the role of PI3K regulatory subunits. PIK3R3, the gene that encodes the PI3K regulatory subunit p55γ, is over-expressed in glioblastoma and ovarian cancers, but its expression in gastric cancer (GC) is not known. We thus used genetic and bioinformatic approaches to examine PIK3R3 expression and function in GC, the second leading cause of cancer mortality world-wide and highly prevalent among Asians. Primary GC and matched non-neoplastic mucosa tissue specimens from a unique Asian patient gastric cancer library were comprehensively profiled with platforms that measured genome-wide mRNA expression, DNA copy number variation, and DNA methylation status. Function of PIK3R3 was predicted by IPA pathway analysis of co-regulated genes with PIK3R3, and further investigated by siRNA knockdown studies. Cell proliferation was estimated by crystal violet dye elution and BrdU incorporation assay. Cell cycle distribution was analysed by FACS. PIK3R3 was significantly up-regulated in GC specimens (n = 126, p < 0.05), and 9.5 to 15% tumors showed more than 2 fold increase compare to the paired mucosa tissues. IPA pathway analysis showed that PIK3R3 promoted cellular growth and proliferation. Knockdown of PIK3R3 decreased the growth of GC cells, induced G0/G1 cell cycle arrest, decreased retinoblastoma protein (Rb) phosphorylation, cyclin D1, and PCNA expression. Using a combination of genetic, bioinformatic, and molecular biological approaches, we showed that PIK3R3 was up-regulated in GC and promoted cell cycle progression and proliferation; and thus may be a potential new therapeutic target for GC.
    BMC Medical Genomics 08/2012; 5(1):34. DOI:10.1186/1755-8794-5-34 · 2.87 Impact Factor
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    ABSTRACT: Salvador promotes both cell cycle exit and apoptosis through the modulation of both cyclin E and Drosophila inhibitor of apoptosis protein in Drosophila. However, the cellular function of human Salvador (hSav1) is rarely reported. To screen for novel binding proteins that interact with hSav1, the cDNA of hSav1 was cloned into a bait protein plasmid, and positive clones were screened from a human fetal liver cDNA library by the yeast two-hybrid system. hSav1 mRNA was expressed in yeast and there was no self-activation and toxicity in the yeast strain AH109. Twenty proteins were found to interact with hSav1, including HS1 (haematopoietic cell specific protein1)-associated protein X-1 (HAX-1); neural precursor cell expressed, developmentally down-regulated 9, pyruvate kinase, liver and RBC, cytochrome c oxidase subunit Vb, enoyl coenzyme A hydratase short chain 1, and NADH dehydrogenase (ubiquinone) 1 beta subcomplex, demonstrating that the yeast two-hybrid system is an efficient method for investigating protein interactions. Among the identified proteins, there were many mitochondrial proteins, indicating that hSav1 may play a role in mitochondrial function. We also confirmed the interaction of HAX-1 and hSav1 in mammalian cells. This investigation provides functional clues for further exploration of potential apoptosis-related proteins in disease biotherapy.
    Molecular Biology Reports 05/2012; 39(8):8225-30. DOI:10.1007/s11033-012-1670-4 · 2.02 Impact Factor
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    ABSTRACT: This study examined the synergetic effect of class IA Phosphoinositide 3-kinases catalytic subunit p110β knockdown in conjunction with oxaliplatin treatment on colon cancer cells. Down-regulation of p110β by siRNA interference and oxaliplatin treatment were applied in colon cancer cell lines HT29, SW620 and HCT116. MTT assay was used to measure the inhibitory effect of p110β knockdown on the proliferation of colon cancer cell lines. SubG1 assay and Annexin-V FITC/PI double-labeling cytometry were applied to detect cell apoptosis. And cell cycle was evaluated by using PI staining and flow cytometry. The expression of caspase 3, cleaved PARP, p-Akt, T-Akt and p110β was determined by western blotting. The results suggested that down-regulation of p110β expression by siRNA obviously reduced cell number via accumulation in G(0)-G(1) phase of the cell cycle in the absence of notablely increased apoptosis in colon cancer cell lines HT29 and SW620 (S phase arrest in HCT116). Moreover, inhibition of p110β expression increased oxaliplatin-induced cell apoptosis and cell cycle arrest in HT29, HCT116 and SW620 cell lines. In addition, increases of cleaved caspase-3 and cleaved PARP induced by oxaliplatin treatment were determined by immunoblotting in p110β knockdown group compared with normal control group and wild-type group. It is concluded that down-regulated expression of p110β could inhibit colon cancer cells proliferation and result in increased chemosensitivity of colorectal cancer cells to oxaliplatin through augmentation of oxaliplatin-induced cell apoptosis and cell cycle arrest.
    Journal of Huazhong University of Science and Technology 04/2012; 32(2):280-6. DOI:10.1007/s11596-012-0049-z · 0.83 Impact Factor
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    ABSTRACT: It has been reported that Salvador (SAV) is a core component of the Salvador-Warts-Hippo (SWH) pathway that restricts cell number, by functioning as a dual regulator of cell proliferation and apoptosis in Drosophila. However, the function of its human ortholog hSav1 (also called hWW45) in mammalian cells is poorly understood. In this study, we identified hematopoietic cell-specific protein 1 (HS1)-associated protein X-1 (HAX1), a 35-kDa protein localized to cell mitochondria, as a novel binding partner of hSav1 using a yeast two-hybrid screening technique. Our finding was confirmed by immunoprecipitation and glutathione-S-transferase (GST) pull-down assays of both proteins. Using immunofluorescence staining, we showed that HAX1 and hSav1 interact with each other. Analysis of the anti-apoptotic function of HAX1 revealed that the presence of hSav1 attenuated the HAX1 protective effects from hydrogen peroxide (H2O2)-induced cell death in MCF-7 cells, while knockdown of hSav1 by small interfering RNAs (siRNAs) significantly enhanced the anti-apoptotic function of HAX1. Also, using the Oncomine database, we found several studies in which HAX1 levels were significantly up-regulated and hSav1 expression was down-regulated in breast cancer samples compared to normal breast tissue. In summary, we conclude that hSav1 interacts with HAX1 and attenuates its protective role against apoptosis in MCF-7 breast cancer cells.
    International Journal of Molecular Medicine 05/2011; 28(3):349-55. DOI:10.3892/ijmm.2011.692 · 2.09 Impact Factor
  • Yu Deng · Guihua Wang · Weina Li · Xiaolan Li · Wei Xiao · Deding Tao · Jianping Gong · Junbo Hu ·
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    ABSTRACT: ObjectiveThe aim of this study was to investigate the sensitivity of chemotherapeutic agents 5-FU, cisplatin (DDP) or TAXOL on colon cancer cell line SW480 with different methods, to find out the best examine time period for further study of chemotherapeutic sensitivities. MethodsThe SW480 cell was treated with 5-FU (200 μg/mL), DDP(150 μg/mL) or TAXOL (50 μg/mL) respectively for 4 h, 8 h or 12 h. MTT assay was used to examine the cell survival rate, Annexin V/PI assay was used to analysis the apoptosis rate, Western Blot assay was applied to examine the expression of apoptotic protein. Results(1) Results of MTT assay showed that the survival rate of SW480 cells at 4h, 8 h or 12 h was: 5-FU (200 μg/mL) 96.0% ± 8.2%, 85.4% ± 7.8%, 74.4% ± 10.2% (P < 0.05); DDP (150 μg/mL) 99.0% ± 6.4%, 88.7% ± 4.7% (P < 0.05), 46.9% ± 2.6% (P < 0.01); TAXOL (50 μg/mL) 51.5% ± 4.2% (P < 0.01), 31.9% ± 3.1%, 17.6% ± 2.3%, or blank group 97.2% ± 5.8%, 98.7% ± 7.2%, 97.5% ± 7.5% respectively. (2) The apoptosis rate of cancer cells at 4 h, 8 h or 12 h was: control group: 3.4% ± 0.2%, 6.2% ± 0.4%, 7.0% ± 0.5%; 5-FU (200 μg/mL) 4.0% ± 0.3%, 4.8% ± 0.4%, 7.7% ± 0.7%; DDP (150 μg/mL) 8.5% ± 0.9%, 18.6% ± 1.6% (P < 0.05), 67.0% ± 6.2% (P < 0.01); or TAXOL (50 μg/mL) 32.0% ± 5.2% (P < 0.01), 76.6% ± 8.5%, 94.0% ± 8.2%, respectively. (3) Western Blot assay showed that the expression of apoptosis associated protein. PARP, X-linked inhibitor of apoptasis (XIAP), Caspase-9 and Bcl-xL were changed. ConclusionThe sensitivity of chemotherapy could be assessed by MTT assay, Annexin V/PI assay and Western Blot. The best examine time of the three chemotherapuc agents was 5-FU (200 μg/mL): > 12 h, DDP(150 μg/mL): 8–12h, or TAXOL (50 μg/mL): < 4 h. Key wordscolon cancer–chemotherapy–sensitivity
    The Chinese-German Journal of Clinical Oncology 05/2011; 10(5):266-269. DOI:10.1007/s10330-011-0772-0
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    ABSTRACT: p55PIK, a regulatory subunit of phosphatidylinositol 3-kinase (PI3K), specifically interacts with retinoblastoma protein (Rb) through the unique NH2 terminus of p55PIK, N24. This interaction is critical for cell proliferation and cell cycle progression. To examine p55PIK as a potential target for cancer therapy, we generated an adenovirus expressing N24 (Ad-N24-GFP) and studied its effects on the proliferation of cultured cancer cells, including human colon (HT29) and thyroid (FTC236) cancer cells. Ad-N24-GFP blocked cell proliferation and induced cell cycle arrest in all cancer cell lines tested. N24 induced cell cycle arrest at G0-G1 phase in cell lines that expressed Rb. Interestingly, N24 inhibited cell proliferation by blocking cell cycle transition at both S and G2-M phases in FTC236 cells, which did not express Rb. When Rb was knocked down by short hairpin RNA in HT29 cells, N24 also inhibited cell cycle progression at S and G2-M phases, suggesting that p55PIK regulates cell cycle progression by Rb-dependent and Rb-independent mechanisms. Finally, Ad-N24-GFP markedly decreased the growth of xenograft tumors derived from HT29 and FTC236 cancer cells in athymic nude mice. Our data strongly suggest that N24 peptide is an effective anticancer therapy, which specifically inhibits PI3K signaling pathways mediated by p55PIK. Moreover, they show that the regulatory subunit of an enzyme, in addition to its catalytic subunit, can be an important target for drug development.
    Molecular Cancer Therapeutics 01/2009; 7(12):3719-28. DOI:10.1158/1535-7163.MCT-08-0499 · 5.68 Impact Factor
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    ABSTRACT: In order to examine the effect of GRIM19 on colon cancer cell SW480, the recombinant adenovirus carrying GRIM19 gene was constructed and transfected into SW480 cells. GRIM19 cDNA was amplified by PCR with the template pcxn2-GRIM19 and cloned into the shuttle plasmid pAdTrack-CMV. The plasmid pAdTrack-CMV-GRIM19 was linearized by PmeI and homologously recombined with bone plasmid pAdEasy-1 in BJ5183, followed by identification by enzyme digestion. After transfection of linearized pAd-GRIM19 with PacI into HEK293 cells, Ad-GRIM19 was obtained and amplified by 3 circles. SW480 cells were infected with Ad-GRIM19. The apoptosis rate was detected by flow cytometry. Agarose electrophoresis revealed the bands of recombinant plasmids identified by enzyme digestion were in the right range corresponding with expectation. Under the fluorescent microscopy, the package of Ad-GRIM19 in HEK293 cells and the expression of Ad-GRIM19 in SW480 cells were observed. The transfection of Ad-GRIM19 into SW480 cells increased the apoptosis rate of SW480 cells as compared with controls. It was concluded that Ad-GRIM19 was successfully constructed and the overexpression of GRIM19 in colon cancer cell lines could promote the apoptotic cell death.
    Journal of Huazhong University of Science and Technology 03/2008; 28(1):14-6. DOI:10.1007/s11596-008-0104-y · 0.83 Impact Factor

Publication Stats

87 Citations
46.43 Total Impact Points


  • 2011-2015
    • Tongji Hospital
      Wu-han-shih, Hubei, China
  • 2008-2014
    • Huazhong University of Science and Technology
      • Department of Surgery
      Wu-han-shih, Hubei, China