miR-411-5p inhibits proliferation and metastasis of breast cancer cell via targeting GRB2.
miR-411-5p (previously called miR-411) is severely involved in human diseases, however, the relationship between miR-411-5p and breast cancer has not been investigated thoroughly. Here, we found that the expression of miR-411-5p was downregulated in breast cancer tissues compared with their matched adjacent non-neoplastic tissues. In addition, the expression of miR-411-5p was also lower in breast cancer cell lines in contrast with MCF-10A. Moreover, we investigated the target and mechanism of miR-411-5p in breast cancer using mimic and inhibitor, and demonstrated the involvement of GRB2 and Ras activation. Ectopic expression of miR-411-5p suppressed the breast cancer cell proliferation, migration and invasion while low expression of miR-411-5p exhibited the opposite effect. Furthermore, GRB2 was demonstrated to be significantly overexpressed in breast cancer tissues compared with normal tissues, and low expression of GRB2 had a longer overall survival compared with high expression of GRB2 in breast cancer. In general, our study shed light on the miR-411-5p related mechanism in the progression of breast cancer and, miR-411-5p/GRB2/Ras axis is potential to be molecular target for breast cancer therapy.
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China; State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen 361102, China.
Yunda
Y
Zhang
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China; Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005, China.
Guoxing
G
Xu
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Gang
G
Liu
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Yongzhi
Y
Ye
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China; State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen 361102, China.
Chuankai
C
Zhang
State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen 361102, China.
Chuannan
C
Fan
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China; Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005, China.
Haibin
H
Wang
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China; Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005, China.
Huali
H
Cai
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China; Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005, China.
Rui
R
Xiao
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China; Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005, China. Electronic address: huangzhengjie@xmu.edu.cn.
Zhengjie
Z
Huang
Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003, China; Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005, China. Electronic address: luoqixmzsh@126.com.
Qi
Q
Luo
D020413:3' Untranslated Regions; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D018450:Disease Progression; D015536:Down-Regulation; D005260:Female; D051380:GRB2 Adaptor Protein / Q000235:genetics* / Q000378:metabolism; D015870:Gene Expression; D020868:Gene Silencing; D006801:Humans; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000235:genetics*; D009361:Neoplasm Invasiveness / Q000235:genetics; D009362:Neoplasm Metastasis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics; D018631:ras Proteins / Q000378:metabolism
D020413:3' Untranslated Regions; D051380:GRB2 Adaptor Protein; C495948:GRB2 protein, human; C582326:MIRN411 microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D018631:ras Proteins
Breast cancer; GRB2; Metastasis; Proliferation; miR-411-5p