Hsa-miR-1 suppresses breast cancer development by down-regulating K-ras and long non-coding RNA MALAT1.
MicroRNAs exert their functions by mainly regulating coding genes or long non-coding RNA expression. In the present study, we reported that hsa-miR-1 was down-regulated in breast cancer tissues. Restoration of miR-1 in breast cancer cells inhibited proliferation, motility and increased apoptosis in vitro. MiR-1 functioned as a tumor suppressor by targeting K-RAS and MALAT1. In addition, the effects of up-regulation of miR-1 were similar to that of silencing K-RAS and MALAT1 in breast cancer cells. In vivo study indicated that restoration of miR-1 inhibited tumor growth and metastasis. Patients with low miR-1 expression had poorer overall survival time than those with high miR-1 expression. Our findings emphasized the potential role of miR-1 as tumor suppressive miRNA in breast cancer.
Department of Thyroid & Breast Surgery, The Third Affiliated Hospital of Sun Yet-sen University, Guangzhou, China.
Ruilei
R
Liu
Department of Thyroid & Breast Surgery, The First Affiliated Hospital of Sun Yet-sen University, Guangzhou, China.
Jie
J
Li
Department of Vascular & Thyroid & Breast Surgery, The First Affiliated Hospital of Sun Yet-sen University, Guangzhou, China.
Yuanhui
Y
Lai
Department of Gastrointestinal Surgery, The Sixth Affiliated Hospital of Sun Yet-sen University, Guangzhou, China.
Yi
Y
Liao
Laboratory of Department of Surgery, The First Affiliated Hospital of Sun Yet-sen University, Guangzhou, China.
Ruiming
R
Liu
Department of Thyroid & Breast Surgery, The Third Affiliated Hospital of Sun Yet-sen University, Guangzhou, China. Electronic address: wsqiu-d@163.com.
Wanshou
W
Qiu
D020413:3' Untranslated Regions; D000328:Adult; D000368:Aged; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D001483:Base Sequence; D001665:Binding Sites; D014408:Biomarkers, Tumor; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D004195:Disease Models, Animal; D015536:Down-Regulation; D000066630:Ectopic Gene Expression; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D035683:MicroRNAs / Q000737:chemistry / Q000235:genetics*; D008875:Middle Aged; D009362:Neoplasm Metastasis; D009367:Neoplasm Staging; D016283:Proto-Oncogene Proteins p21(ras) / Q000737:chemistry / Q000235:genetics*; D034622:RNA Interference; D062085:RNA, Long Noncoding / Q000737:chemistry / Q000235:genetics*; D012333:RNA, Messenger / Q000737:chemistry / Q000235:genetics; D047368:Tumor Burden / Q000235:genetics; D023041:Xenograft Model Antitumor Assays
D020413:3' Untranslated Regions; D014408:Biomarkers, Tumor; C117307:KRAS protein, human; C557041:MALAT1 long non-coding RNA, human; C544547:MIRN1 microRNA, human; D035683:MicroRNAs; D062085:RNA, Long Noncoding; D012333:RNA, Messenger; D016283:Proto-Oncogene Proteins p21(ras)
K-RAS; MALAT1; miR-1