miR-221/222靶向抑制对三阴性乳腺癌MDA-MB-231细胞顺铂敏感性的影响

Abstract
Figure/Table
References (25)
Related Citation (15)

Download: PDF (709 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the Cisplatin (DDP) sensitivity of microRNA (miR)-221/222 targeted inhibition on triple-negative breast cancer (TNBC) MDA-MB-231 cells. Methods MDA-MB-231 cells were randomly divided into control group, miR-221 inhibition group, miR-222 inhibition group and miR-221/222 inhibition group, transfected with blank reagent, miR-221 inhibitor, miR-222 inhibitor and miR-221/222 inhibitor respectively, and after transfection, DDP 5 μg/mL was given for culture. Relative expression of miR-221/222 mRNA was detected by fluorescence quantitative polymerase chain reaction, inhibition rate of cell proliferation was detected by MTT method, apoptosis rate was detected by Annexin V-FTTC/PI double staining method, and the expression levels of apoptosis related proteins were detected by Western blot. Results Comparing the expression level of miR-221 mRNA, the miR-221 inhibition group was lower than the control group, the miR-222 inhibition group was higher than the miR-221 inhibition group, and the miR-221/222 inhibition group was lower than the miR-222 inhibition group, and the differences were statistical significance (all P ＜ 0.05). The expression level of miR-222 mRNA in the miR-222 inhibition group and miR-221/222 inhibition group were lower than that of the miR-221 inhibition group and the control group, and the differences were statistically significant (all P ＜ 0.05). The inhibition rate of cell proliferation and apoptosis of the miR-221/222 inhibition group was higher than that of the other three groups at 24 and 48 h after transfection, and the differences were statistically significant (all P ＜ 0.05). The levels of Caspase-9 and Bax in the miR-221/222 inhibition group were higher than those of the other three groups at 48 h after transfection, and the Bcl-2 level was lower than that of the other three groups, and the differences were statistically significant (all P ＜ 0.05). Conclusion Co-inhibition of miR-221/222 can increase DDP sensitivity of MDA-MB-231 cells.

Key words： Triple-negative breast cancer Cisplatin miR-221 miR-222 Sensitivity

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	YE Huirong YUAN Huiling CAO Yin WANG Xiyue WU Lihua CHEN Guilin CHEN Lijuan ZHANG Yujuan▲

Cite this article:

YE Huirong YUAN Huiling CAO Yin WANG Xiyue WU Lihua CHEN Guilin CHEN Lijuan ZHANG Yujuan▲. Effect of miR-221/222 targeted inhibition on Cisplatin sensitivity of triple-negative breast cancer MDA-MB-231 cells[J]. 中国医药导报, 2020, 17(35): 23-26,41.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2020/V17/I35/23

[1] Wang H，Qin RL，Cheng YQ. LncRNA-Ang362 Promotes Pulmonary Arterial Hypertension by Regulating miR-221 and miR-222 [J]. Shock，2020，53（6）：723-729.
[2] Li B，Lu Y，Yu L，et al. miR-221/222 promote cancer stem-like cell properties and tumor growth of breast cancer via targeting PTEN and sustained Akt/NF-κB/COX-2 activation [J]. Chem Biol Interact，2017，277：33-42.
[3] Liang YK，Lin HY，Dou XW，et al. MiR-221/222 promote epithelial-mesenchymal transition by targeting Notch3 in breast cancer cell lines [J]. NPJ Breast Cancer，2018，4（1）：1-9.
[4] Gorbatenko A，S?覬kilde R，Sorensen EE，et al. HER2 and p95HER2 differentially regulate miRNA expression in MCF-7 breast cancer cells and downregulate MYB proteins through miR-221/222 and miR-503 [J]. Sci Rep，2019，9（1）：1-16.
[5] 张春智，康春生，杨卫东，等.共抑制miR-221/222表达上调PUMA促进胶质瘤U251细胞凋亡的体外研究[J].中华神经外科杂志，2010（8）：752-755.
[6] Liu S，Wang Z，Liu Z，et al. miR-221/222 activate the Wnt/β-catenin signaling to promote triple-negative breast cancer [J]. J Mol Cell Biol，2018，10（4）：302-315.
[7] Abo ElAtta AS，Ali YBM，Bassyouni IH，et al. Upregulation of miR-221/222 expression in rheumatoid arthritis（RA）patients：correlation with disease activity [J]. Clin Exp Med，2019，19（1）：47-53.
[8] Liu H，Cao B，Zhao Y，et al. Upregulated miR-221/222 promotes cell proliferation and invasion and is associated with invasive features in retinoblastoma [J]. Cancer Biomark，2018，22（4）：621-629.
[9] Liu Q，Zhou Q，Zhong P. circ_0067934 increases bladder cancer cell proliferation，migration and invasion through suppressing miR-1304 expression and increasing Myc expression levels [J]. Exp Ther Med，2020，19（6）：3751-3759.
[10] Chai WH，Li YR，Lin SH，et al. Antihelminthic niclosamide induces autophagy and delayed apoptosis in human non-small lung cancer cells in vitro and in vivo [J]. Anticancer Res，2020，40（3）：1405-1417.
[11] Steed KL，Jordan HR，Tollefsbol TO. SAHA and EGCG Promote Apoptosis in Triple-negative Breast Cancer Cells，Possibly Through the Modulation of cIAP2 [J]. Anticancer Res，2020，40（1）：9-26.
[12] 肖奕，马大昌，王红磊，等.基于ATP7A探讨粉防己碱对乳腺癌细胞顺铂耐药的逆转作用及机制[J].中国医药导报，2018，15（34）：18-22.
[13] 秦明明，浦春，冯钢，等.let-7i通过抑制K-Ras、Bcl2的表达降低乳腺癌细胞化疗耐药性[J].细胞与分子免疫学杂志，2019，35（11）：992-999.
[14] Lee JO，Kang MJ，Byun WS，et al. Metformin overcomes resistance to cisplatin in triple-negative breast cancer（TNBC）cells by targeting RAD51 [J]. Breast Cancer Res，2019，21（1）：115.
[15] 陈霁晖，顾芬芬，李超，等.ABC跨膜转运蛋白基因表达与乳腺癌铂类药物敏感性的相关性研究[J].药学与临床研究，2019，27（2）：93-97.
[16] Rocha CRR，Silva MM，Quinet A，et al. DNA repair pathways and cisplatin resistance：an intimate relationship [J].Clinics：Sao Paulo，2018，73（suppl 1）：e478s.
[17] Sun CY，Nie J，Huang JP，et al. Targeting STAT3 inhibition to reverse cisplatin resistance [J]. Biomed Pharmacother，2019，18（117）：109135.
[18] 陈永胜，黄丹青，谷依学，等.APOBEC3B介导非小细胞肺癌顺铂耐药[J].中国医师杂志，2020，22（5）：662-666， 673.
[19] Abu N，Hon KW，Jeyaraman S，et al. Long noncoding RNAs as biotargets in cisplatin-based drug resistance [J]. Future Oncol，2018，14（29）：3085-3095.
[20] Sun T，Du SY，Armenia J，et al. Expression of lncRNA MIR222HG co-transcribed from the miR-221/222 gene promoter facilitates the development of castration-resistant prostate cancer [J]. Oncogenesis，2018，7（3）：30.
[21] Gorbatenko A，S?覬kilde R，Sorensen EE，et al. HER2 and p95HER2 differentially regulate miRNA expression in MCF-7 breast cancer cells and downregulate MYB proteins through miR-221/222 and miR-503 [J]. Sci Rep，2019，9（1）：3352.
[22] Xie Q，Yan YR，Huang ZP，et al. MicroRNA-221 targeting PI3-K/Akt signaling axis induces cell proliferation and BCNU resistance in human glioblastoma [J]. Neuropathology，2014，34（5）：455-64.
[23] Li W，Guo F，Wang P，et al. miR-221/222 confers radioresistance in glioblastoma cells through activating Akt independent of PTEN status [J]. Curr Mol Med，2014，14（1）：185-95.
[24] Yang JK，Yang JP，Tong J，et al. Exosomal miR-221 targets DNM3 to induce tumor progression and temozolomide resistance in glioma [J]. J Neurooncol，2017，131（2）：255-265.
[25] Rao X，Di Leva G，Li M，et al. MicroRNA-221/222 confers breast cancer fulvestrant resistance by regulating multiple signaling pathways [J]. Oncogene，2011，30（9）：1082-1097.