The anti-apoptotic effect of cytoplasmic alpha-fetoprotein in hepatoma cells induced by all-trans retinoic acid involves activation of the PI3K/AKT signaling pathway / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To explore the effect of alpha-fetoprotein (AFP) on transduction of the PI3K/ AKT signal in hepatocellular carcinoma cells and the role played by AFP in resistance to cytotoxicity of all-trans retinoic acid (ATRA).</p><p><b>METHODS</b>The effects of ATRA of human liver cancer cells was assessed using the BEL-7402 cell line with the MTT assay (to evaluate proliferation), microscopy (to evaluate morphology), flow cytometry (to evaluate apoptosis), laser confocal microscopy and coimmunoprecipitation (co-IP; to evaluate co-localization and interaction of AFP with PTEN), Western blotting (to evaluate expression of phosphorylated-protein kinase B (pAKT) and Src, and RNA interference (RNAi)-mediated knockdown of AFP. Finally, application of the PI3K-specific inhibitor Ly294002 was used to monitor the influence of AFP in transduction of the PI3K signal pathway.</p><p><b>RESULTS</b>The human hepatoma cell line BEL-7402 were resistant to ATRA cytotoxicity. PTEN and AFP co-localized in the cytoplasm, and co-IP indicated that AFP interacts with PTEN in BEL-7402 cells.RNAi knockdown of AFP expression led to reduced growth of BEL-7402 cells.BEL-7402 cells transfected with AFP-short interfering (si)RNA vectors showed enhanced sensitivity to ATRA and reduced expression of pAKT(Ser473) and Src; Ly294002 reduced the role of AFP in stimulating expression of pAKT(Ser473) and Src.</p><p><b>CONCLUSION</b>AFP can activate transduction of the PI3K/AKT signal, and expression of AFP in hepatoma cells is a pivotal event for resisting ATRA-induced apoptosis.</p>

Clinical study of tissue expression and serum contents of VEGF-C in cervical diseases of Uighur women / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To detect the VEGF-C expression in the serum and tissue of cervical diseases. To explore correlation of tissue and serum expression and the clinical significance of VEGF-C in the cervical intraepithelial neoplasia and cervical squamous-celled carcinoma of Uighur momen in Xinjiang.</p><p><b>METHOD</b>(1) The VEGF- C expressions in tissue were tested by immunohistochemisty from the 22 chronic cervicitis, 24 CIN,and 43 squamous-celled carcinoma patients, (2) The VEGF-C contents in the serum were tested by enzyme-linked immunosorbent assay (ELISA) from the 15 chronic cervicitis, 23 CIN, and 40 squamous-celled carcinoma patients.</p><p><b>RESULT</b>(1) The expression of VEGF-C in the tissue of cervicitis, CIN and cervical carcinoma were separately 9.1%, 87.50%, 100%, the differences had significance (P < 0.05). (2) The VEGF-C serum contents were gradually increased from cervicitis to CIN and cervical carcinoma, the differences had significance (P < 0.05). (3) The compartment of results of VEGF-C in serum and tissue showed that, there were correlation between to of them, the more tissue expressions, the more serum expressions will be (r = 0.27, F = 5.327, P < 0.05).</p><p><b>CONCLUSION</b>VEGF-C has played an facilitation rule in the transition process of CIN to cervical squamous cell carcinoma of the Uygure women in Xinjiang, there are correlation of VEGF-C expression between tissue and serum.</p>

Study on the correlation of Xinjiang endometrial tumor and vascular endothelial growth factor / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To explore the relationships of serum vascular endothelial growth factor (VEGF) and endometrial cancer of Uighur Women in Xinjiang.</p><p><b>METHODS</b>The serum of 50 endometrial cancer patient's and 70 healthy women' s were collected. VEGF expressions were tested by ELISA method and the correlations of endometrial cancer with VEGF were analysed. The variety of serum VEGF in different clinical stages of endometrial cancer was analyzed.</p><p><b>RESULTS</b>Serum VEGF expressions on endometrial cancer were significantly higher than normal ones (P < 0.01); The serum VEGF level in late stage was significantly higher than early stage (P < 0.01). The serum VEGF level significantly increased from well differentiated to the poorly differentiated cases (P < 0.05).</p><p><b>CONCLUSION</b>high level expressions of VEGF are related to the endometrial cancer. Uighur Women in Xinjiang, particularly high expressed in advanced and poorly differentiated endometrial cancer.</p>

Effects of alpha-fetoprotein on the expression of TRAIL death receptor-2 and its role on resisting the cytotoxicity of TRAIL in hepatoma cells / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To explore the mechanism of Alpha-fetoprotein (AFP) effects on hepatocellular carcinoma cells (HCC) resistances apoptosis induced by tumor necrosis factor-related apoptosis inducing-ligand (TRAIL).</p><p><b>METHODS</b>The expressed alteration of TRAIL receptor-2 (DR5) after the human hepatoma cells line Bel 7402 (AFP-producing) and HLE cells (non-AFP producing) were treated with all trans retinoic acid (ATRA) were determined by Western blot; Interaction of AFP with RAR-beta was analyzed by co-immunoprecipitation (Co-IP); Laser confocal microscopy was used to observe co-localization of AFP and RAR-beta; Short small RNA interfering (RNAi) was applied to knock down the expression of AFP in Bel 7402 cells; The full AFP gene cDNA was inserted into pcDNA3.1 vector and constructed the expressed vector of AFP (named pcDNA3.1-afp); The growth of hepatoma cells was analyzed by MTT.</p><p><b>RESULTS</b>Bel 7402 and HLE cells expressed DR5, lowed dosage of ATRA (40mumol/L) had no influence on the expression of DR5 in Bel 7402 cells, but ATRA (160mumol/L) could inhibit the expression of AFP and promote the expression of DR5 significantly; Co-IP indicated that AFP had a property for interacting with RAR-beta; The results also demonstrated AFP co-localization with RAR-beta in cytoplasm of Bel 7202 cells; The expression of DR5 was enhanced while the expression of AFP was knocked down by RNAi. pcDNA3.1-afp vector was transfected into HLE cells, the growth of HLE cells were stimulated and TRAIL cytotoxicity of HLE cells were reduced. But when the expression of AFP was knocked down the sensitivity of Bel 7402 cells to TRAIL was enhanced.</p><p><b>CONCLUSIONS</b>These data provided that AFP had a capability to interact with RAR-beta and suppressed the expression of DR5. AFP could play pivotal role on hepatoma cells resistance-induced apoptosis by TRAIL.</p>