Objective To investigate the effect and the possible mechanism of osthole on proliferation and apopotosis of human cervical carcinoma Hela cells and its passible mechanism.Methods After cervical carcinoma Hela cells were incubated with different concentrations osthole,the cell proliferation activity was examined by MTT assay.The apoptosis rate and cellular ROS level were measured by flow cytometry.The Bcl-2 and Bax mRNA expression was determined by semi-quantitative RT-PCR.Results In comparison with the control group,osthole with different concentrations could obviously inhibit the Hela cells proliferation and accelerated the cellular apoptosis,lowered the expression rate of Bcl-2/Bax,raise the cellular ROS level in a osthole dose-dependent manner.Conclusion Osthole may inhibit Hela cell proliferation and accelerates the cells apoptosis,which might be associated with the increasing the cellular ROS level,promoting Bax expression and inhibiting Bcl-2 expression.

OBJECTIVE To investigate the role of solute carrier family 1 member 4(SLC1A4) in platinum-based chemotherapy resistance in ovarian cancer. METHODS The expression of SLC1A4 in ovarian cancer or platinum-resistant ovarian cancer was analyzed by GEO and TCGA database analysis tools. The expression of SLC1A4 in platinum-treated ovarian cancer cell lines was analyzed by GEO database. The relation of SLC1A4 expression and overall survival(OS) or progression free survival(PFS) in ovarian cancer patients were analyzed by Kaplan Meier-plotter. Correlation between SLC1A4 gene effect and sensitivity to chemotherapeutic agents in ovarian cancer was analyzed through DepMap platform. Low expression of SLC1A4 mediates cisplatin resistance in ovarian cancer cells as verified by flow cytometry and tumor cell clone colony formation assays; prediction of microRNAs(miRNA) targeting SLC1A4 was conducted using TargetScan then validated their correlation in TCGA ovarian cancer samples. Used COREMINE tool to analyze the biological processes of SLC1A4 mediating chemoresistance in ovarian cancer. RESULTS SLC1A4 was significantly reduced in ovarian cancer patients and platinum-resistant ovarian cancer(P<0.05) and significantly correlated with OS and PFS in ovarian cancer patients(P<0.05). SLC1A4 expression was increased in ovarian cancer cells with platinum treatment. The genetic effect of SLC1A4 on ovarian cancer was positively correlated with platinum drug sensitivity. Overexpression of SLC1A4 increased cisplatin-induced apoptosis and reduced tumor cell colony formation in ovarian cancer cells. Hsa-let-7c-5p was targeted to SLC1A4 and significantly negatively correlated in samples from drug-resistant ovarian cancer patients. CONCLUSION Low expression of SLC1A4 mediates platinum drug resistance in ovarian cancer and is potentially associated with hsa-let-7c-5p regulation.