[Expression of MiR-130a in Serum Samples of Patients with Epithelial Ovarian Cancer and Its Association with Platinum Resistance].

OBJECTIVE: To determine the expression of miR-130a in patients with epithelial ovarian cancer and its association with platinum resistance. METHODS: 32 patients with platinum resistance and 30 patients without platinum resistance were recruited in this study. Real-time PCR was performed to detect the expression of miR-130a in the serum samples of the patients. ELISA was used to measure the expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN) and B-cell lymphoma-2 (BCL-2). RESULTS: Platinum-resistant patients had significantly higher levels of expression of miR-130a and BCL-2, and lower level of PTEN than platinum-sensitive patients (P < 0.05). The expression level of miR-130a increased with increased severity in histological classification and appearance of lymph node metastasis in the platinum-resistant patients (P < 0.05). CONCLUSION: MiR-130a may mediate the generation of platinum resistance in epithelial ovarian cancer through inhibiting PTEN to activate PI3K/AKT signaling pathway and increasing BCL-2 to inhibit tumor cell apoptosis. MiR-130a may be a new potential target of gene therapy in platinum-resistant ovarian cancers.

[Regulatory effects and associated mechanisms of miR-130a molecules on cisplatin resistance in ovarian cancer A2780 cell lines].

OBJECTIVE: To determine the regulatory effects and associated mechanisms of miR-130a on cisplatin resistance in ovarian cancer A2780 cell lines (including cisplatin sensitive A2780s and its resistant A2780/DDP cells). METHODS: A2780s and A2780/DDP cells were divided into four groups, and treated with lipo2000 (Lip), miR-negative (miR-NC) control, miR-130a-mimics (miR-130a-M increasing the expression of miR-130a and the agent), and miR-130a-inhibitor (miR-130a-I downregulating miR-130a expression), respectively. The proliferation of cells and their sensitivity to cisplatin were detected by MTT assay. RT-PCR and western blot were performed to examine the levels of MDR1, PTEN mRNA and proteins. RESULTS: The expressions of MDR1 mRNA and P-gp in the A2780/DDP cells were significantly higher than those in the A2780s cells. However, no differences in the expressions of PTEN mRNA and proteins were detected between the two cell lines. Over-expressions of miR-130a had no effect on cell proliferation, but increased the resistance of the cells to cisplatin and up-regulated the expressions of MDR1 mRNA and P-gp in both cell lines. Down-regulated miR-130a did not affect cell proliferations, but enhanced the sensitivity of the cells to cisplatin, inhibited the expressions of MDR1 mRNA and P-gp and increased the expression of PTEN proteins. CONCLUSION: MiR-130a expression may be associated with cisplatin resistance of ovarian cancer cells. MiR-130a inhibitor can reverse the cisplatin resistance by upregulating the expression of PTEN proteins and down-regulating P-gp in A2780 cell lines. MiR-130 may become a new potential target of genetic therapy for cisplatin-resistant ovarian cancers.

[Expression of miR-130a in cisplatin resistant cell lines of ovarian cancer].

OBJECTIVE: To determine the expression of miR-130a in cisplatin resistant cell lines of ovarian cancer and its impact on cisplatin resistance. METHODS: Cisplatin resistant ovarian cancer cell lines were established by stepwise selection with gradual increase of cisplatin. MTT assay was applied to indentify the cisplatin resistant cell lines and determine their resistance index. The expression of miR-130a was measured by SYBR green real-time PCR. RESULTS: The resistance index of A2780/CIS1, A2780/CIS2 and SKOV3/CIS was 30.2, 5.3 and 24.5 respectively. The SYBR green real-time PCR showed that miR-130a was over-expressed in all of the cisplatin resistant cell lines (P < 0.05). The expression of miR-130a was 30.51 times higher in A2780/CIS1, 4.87 times higher in A2780/CIS2 and 24.43 times higher in SKOV3/CIS than in their parental cell lines (P < 0.05), which was almost equally reflected in their resistance index. CONCLUSION: The over expression of miR-130a is associated with cisplatin resistance of ovarian cancer. Inhibiting miR-130a expression may help reverse the cisplatin resistance of ovarian cancer. miR-130a is expected to be a new potential target of genetic therapy for cisplatin resistant ovarian cancer.

[Inhibition effect and mechanism of artemisnin on surgically induced endometriosis].

OBJECTIVE: To evaluate the inhibitory effect of artemisnin on surgically induced endometriosis in rat model and the possible mechanism related to cellular apoptosis and microvascular angiogenesis. METHODS: Surgically induced endometriosis model was established with female rats, and then the rats were divided into four groups: high dose artemisinin [300 mg/(kg x d)), low dose artemisinin [150 mg/(kg x d)], danazol [160 mg/(kg x d)] and solvent control group After daily administration of the above agents for 4 weeks, the rats were sacrificed, then the implant size of ectopic endometrium was measured and appotosis index (AI), Bcl-2 and MVD in ectopic endometrium were evaluated with S-P immunohistochemistry. RESULTS: Compared with solvent control, both artemisinin (high and low quality) and danazol decrease the size of implants significantly (P < 0.05), and there was no significant difference among the three treatment groups. AI of the three treatment groups increased significantly, while Bcl-2 and MVD decreased significantly (P < 0.05). AI of both artemisinin groups were significantly higher than that of danazol group, but Bcl-2 level was lower. CONCLUSION: Artemisnin inhibits surgically induced endometriosis in rats, and the possible mechanism may be related to stimulatation of cellular apoptosis and inhibition of angiogenesis.