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Effects of miR-1203 and HOTAIR SNP rs7958904 on the growth of breast cancer cells |
LIU Wenhui1 XIAO Jian2 SUN Weihua3 YANG Na3 LIU Boxuan3 GONG Jianping3 |
1.Department of Pharmacy, the Second Xiangya Hospital of Central South University, Hu'nan Province, Changsha 410008, China;
2.Department of Pharmacy, Xiangya Hospital of Central South University, Hu'nan Province, Changsha 410008, China;
3. Department of Pharmacy, Huaihua Second People's Hospital, Hu'nan Province, Huaihua 418000, China |
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Abstract Objective To investigate the association between genetic variation of lncRNA HOTAIR SNP rs7958904 and miR-1203, as well as to explore their roles in the growth of breast cancer (BC) cells. Methods The wild type and mutant HOTAIR SNP rs-7958904 were both cloned into the Dual-Luciferase Reporter Vector and Over-expression vector, respectively. The Dual-Luciferase Reporter Vectors and miR-1203 mimics were co-transfected into the cells, and then the luciferase expression was detected. Furthermore, BC cells were transfected with the overexpression vector and/or miR-1203 mimics/inhibitors. And then, HOTAIR expression was detected by fluorescent quantitative PCR, cell proliferation was assessed by BrdU, cell apoptosis was tested by Annexin V-FITC/PI, and cell invasion was examined by Transwell Assay. Results The binding of miR-1203 and HOTAIR was enhanced by mutant HOTAIR; miR-1203 could down-regulate the expression of mutant HOTAIR (P < 0.01), but such down regulation on wild-type HOTAIR was insignificant (P > 0.05). The wild-type HOTAIR promoted the proliferation and invasion of BC cells significantly but inhibit their apoptosis (P < 0.01); whereas such effect of the mutant HOTAIR declined obviously and could be blocked by miR-1203. miR-1203 had the opposite effect of HOTAIR; when the expression of miR-1203 was inhibited, the mutant HOTAIR exhibited a similar effect as wild-type HOTAIR. Conclusion The mutant HOTAIR rs7958904 can down-regulate the activity of HOTAIR, and such down regulation may probably associated with the increment of miR-1203 binding sites. This finding could provide a new direction for the future study in the function of lncRNA SNPs.
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