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作 者:李冰[1] 邹晓明[1] 董长城[1] 赵金[1] LI Bing;ZOU Xiao-ming;DONG Chang-cheng;ZHAO Jin(Department of General Surgery,Baogang Hospital of Inner Mongolia,Baotou 014010,China)
机构地区:[1]内蒙古包钢医院普外科,内蒙古包头014010
出 处:《中国现代普通外科进展》2021年第7期510-513,共4页Chinese Journal of Current Advances in General Surgery
摘 要:目的 :探讨miR-558调控乳腺癌细胞凋亡的潜在机制。方法:用miR-558 inhibitor敲低miR-558或miR-558 mimics过表达miR-558后,检测乳腺癌细胞BC-009、MCF-7、MDA-MB-435、MX-1、BT-20、HCC1937的凋亡水平。通过miRDB在线分析和荧光素酶报告系统确定miR-558的靶标。通过过表达或敲低靶标检测其是否影响乳腺癌细胞MCF-7的凋亡水平。结果:敲低miR-558后,乳腺癌细胞BC-009、MCF-7、MDA-MB-435、MX-1、BT-20、HCC1937的凋亡水平下降(P<0.05);过表达miR-558后,上述乳腺癌细胞凋亡水平上升(P<0.05)。miRDB在线分析发现miR-558潜在靶向HOXA1、CGREF1、CD155、ZNF217、RNF19A、DIS3L2、TMEM140、DPYSL2、COPS2、HM GB2。敲低miR-558后,CD155的表达量上升(P<0.05);过表达miR-558后CD155则表达量下降(P<0.05)。荧光素酶报告系统发现miR-558靶向CD155的3端非编码区(P<0.05)。敲低CD155后,乳腺癌细胞MCF-7的凋亡水平上升(P<0.05)。过表达CD155后,则水平下降(P<0.05),同时过表达miR-558和CD155,或同时敲低miR-558和CD155,凋亡水平无明显变化(P>0.05)。结论:miR-558通过靶向CD155的mRNA的3端非编码区抑制CD155的蛋白水平,促进了乳腺癌细胞的凋亡。Objective: To investigate the potential mechanism of miR-558 in regulating breast cancer cell apoptosis. Methods: miR-558 inhibitor was used to knock down miR-558 or miR-558 mimics to overexpress miR-558, and then detect breast cancer cells BC-009, MCF-7,MDA-MB-435, MX-1, BT-20, HCC1937 apoptosis level. The target of miR-558 was determined by miRDB online analysis and luciferase reporting system. It was detected by overexpression or knockdown of the target whether it affects the apoptosis level of breast cancer cell MCF-7. Results: After miR-558 was knocked down, the apoptosis levels of breast cancer cells BC-009, MCF-7,MDA-MB-435, MX-1, BT-20, and HCC1937 decreased(P<0.05);overexpression of miR-After 558,the apoptosis levels of breast cancer cells BC-009, MCF-7, MDA-MB-435, MX-1, BT-20, and HCC1937 increased(P<0.05). Online analysis of miRDB revealed that miR-558 potentially targets HOXA1, CGREF1, CD155, ZNF217, RNF19 A, DIS3 L2, TMEM140, DPYSL2, COPS2, HMGB2. After miR-558 was knocked down, the expression of CD155 was increased(P<0.05);after overexpression of miR-558, the expression of CD155 was found to be decreased(P<0.05). The luciferase reporter system found that miR-558 targeted the non-coding region at the 3 ends of CD155(P<0.05). After knocking down CD155, the apoptosis level of breast cancer cell MCF-7 increased(P<0.05). After overexpression of CD155, the apoptosis level of breast cancer cell MCF-7 was decreased(P<0.05).Overexpression of miR-558 and CD155 at the same time did not significantly change the apoptosis level of breast cancer cell MCF-7(P>0.05);while miR-558 and CD155 were knocked down, there was no significant change in the apoptosis level of breast cancer cell MCF-7(P>0.05). Conclusion:miR-558 inhibits the protein level of CD155 by targeting the non-coding region of the 3-terminus of CD155 mRNA, and ultimately promotes the apoptosis of breast cancer cells.
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