ABSTRACT
Objective To explore the effect of miR-200b on chemosensitivity of cervical cancer HeLa cells to paclitaxel and its mechanism.Methods A recombinant miR-200b mimics was transfected into cultured HeLa cells,which were divided into observation group,negative group,and blank control group.Each group was treated with different concentrations of paclitaxel.Methyl thiazolyl tetrazolium (MTF) assay was performed to evalate the proliferative ability of these treated cells to paclitaxel.AnnexinVFITC/PI method was used to detect the apoptosis rate of Hela cells.The protein level of vascular endothelial growth factor (VEGF) was detected by Western blot.Results MTT assay showed that the OD values of three groups were totally different;and compared to the other two groups,the OD value of the transfected HeLa cells was significantly lower (P ＜ 0.05).Compared to the negative group and the blank control group,there was no statistical difference (P ＞ 0.05).AnnexinV-FITC/PI results demonstrated that the apoptotic index of the transfected HeLa cells was significantly higher than that in the other two groups (P ＜0.05).Western blot assay showed that expression of VEGF protein in three groups of relative quantity was 0.403 ± 0.046,0.882 ± 0.094,and 0.901 0.102,respectively.There was significant difference among there groups (P ＜ 0.05).Conclusions miR-200b mimics can increase the sensitivity of cervical cancer HeLa cells to paclitaxel,and targeted regulation of VEGF may be the cause of increasing in drug sensitivity.
ABSTRACT
Objective To investigate the expression of the hsa-miR-155 in serum of endometrial cancer and its clinical significance. Methods Collected 44 cases blood specimens before surgery operation from Sep. 2008 to Dec. 2009, and collected 12 cases blood specimens from the health of volunteers in comparison. Real time quantity PCR was used to detect the expression of hsa-miR-155 in those specimens and analyzed clinical pathological with the expression of hsa-mir-155 in endometrial cancer. Results The expression of hsa-miR-155 was (3.9 ±0.7) in endometrial cancer, which was significantly higher than that in control group( P ＜ 0.01 ). The expressions of hsa-miR-155 were ( 3.7 ± 0.6 ), ( 3.9 ± 0.6 ) and ( 3.7 ±0.6)times in well, moderately and poorly differentiated endometrial cancer, respectively,while there were not significant difference ( P ＞ 0.05 ). The expressions were ( 3.8 ± 0.6 ) and ( 3.9 ± 0.6 ) times between endometrioid adenocarcinoma and non-endometrioid adenocarcinoma, and there were significant difference (P ＞ 0.05). The expressions were ( 2.1 ± 0.4 ) and ( 5.6 ± 0.8 ) times in stage Ⅰ - Ⅱ and Ⅲ - Ⅳ endometrial cancer, respectively, in which there were significant difference (P ＜ 0.05 ). The expressions of hsa-miR-155 were (5.5 ± 0.5 ) and ( 1.9 ± 0.2) times between lymph node metastasis and without lymph node metastasis in endometrial cancer, in which there were significant difference (P ＜ 0.01 ). Conclusion Hsa-miR-155 may play an important role in the proliferation, and metastasis of endometrial cancer, which may be a indicator in the diagnosis and prognosis of endometrial cancer and may be used as a predictive biomarker.