miR-1296-5p decreases ERBB2 expression to inhibit the cell proliferation in ERBB2-positive breast cancer.
miR-1296-5p decreases ERBB2 expression to inhibit the cell proliferation in ERBB2-positive breast cancer.
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miR-1296-5p降低ERBB2表达以抑制ERBB2阳性乳腺癌细胞增殖
DOI：
10.1186/s12935-017-0466-y
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发表时间：
2017
影响因子：
5.8
通讯作者：
Zhu Y
中科院分区：
文献类型：
--
作者：
Chen G;He M;Yin Y;Yan T;Cheng W;Huang Z;Zhang L;Zhang H;Liu P;Zhu W;Zhu Y
BackgroundThe tumor suppressive role of miR-1296 is observed in triple negative breast cancer (TNBC). However, the effect of miR-1296-5p in ERBB2-positive breast cancers remains obscure.MethodsWhetherERBB2was the target gene of the miR-1296-5p was predicted by online software, and determined by dual-luciferase activity assay. miR-1296-5p expression levels were determined in breast cancer samples (114 breast cancer tissues and 30 adjacent normal tissues) by using qRT-PCR. The effect of miR-1296-5p and inhibition of ERBB2/mTORC1 signaling on the downstream target was assessed by Western blot. SK-BR-3 and BT-474 breast cancer cell line was transfected with miR-1296-5p mimic after which cell proliferation and apoptosis were determined by the clonogenic assay and the flow cytometry system, respectively. In addition, the chemotherapeutic drug sensitivity of SK-BR-3 and BT-474 cells transfected with miR-1296-5p mimic were determined by MTT assay.ResultsThe luciferase assay carrying ERBB2 3′-untranslated region-based reporters expressed in SK-BR-3 and BT-474 cells suggested thatERBB2was the target gene of miR-1296-5p. MiR-1296-5p was significantly decreased in breast cancer tissues compared to adjacent normal tissues. Moreover, it was declined in ERBB2-positive breast cancer samples compared with that in ERBB2-negative breast cancer tissues. Overexpressed miR-1296-5p reduced its target protein level and mTORC1/S6 activation, inhibited the proliferation of ERBB2-positive breast cancer cells and sensitized these cells to cisplatin and 5-fluorouracil-induced apoptosis.ConclusionsOur findings suggest that miR-1296-5p is involved in the regulation of proliferation in breast cancer cells via targeting ERBB2/mTORC1 signaling pathway.
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影响因子：
9.2
作者：
Boo L;Ho WY;Ali NM;Yeap SK;Ky H;Chan KG;Yin WF;Satharasinghe DA;Liew WC;Tan SW;Ong HK;Cheong SK
通讯作者：
Cheong SK
DOI：
10.1200/jco.2016.67.4887
发表时间：
2017-01-10
期刊：
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
影响因子：
--
作者：
Perez EA;Barrios C;Eiermann W;Toi M;Im YH;Conte P;Martin M;Pienkowski T;Pivot X;Burris H 3rd;Petersen JA;Stanzel S;Strasak A;Patre M;Ellis P
通讯作者：
Ellis P
影响因子：
--
作者：
Liu Z;He W;Gao J;Luo J;Huang X;Gao C
通讯作者：
Gao C
影响因子：
45.3
作者：
Thavendiranathan, Paaladinesh;Amir, Eitan
通讯作者：
Amir, Eitan
影响因子：
45.3
作者：
Urruticoechea, Ander;Rizwanullah, Mohammed;Munoz, Montserrat
通讯作者：
Munoz, Montserrat