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RETRACTION: Long noncoding RNA linc‐ITGB1 promotes cell migration and invasion in human breast cancer
Author(s) -
Yan Meidi,
Zhang Lina,
Li Guoqing,
Xiao Shengwen,
Dai Ji,
Cen Xueying
Publication year - 2016
Publication title -
biotechnology and applied biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.468
H-Index - 70
eISSN - 1470-8744
pISSN - 0885-4513
DOI - 10.1002/bab.1461
Subject(s) - gene knockdown , breast cancer , cancer research , epithelial–mesenchymal transition , biology , cancer , cell growth , small hairpin rna , metastasis , cell cycle , long non coding rna , vimentin , carcinogenesis , downregulation and upregulation , cell culture , immunology , genetics , immunohistochemistry , gene
RETRACTION: Breast cancer is the most commonly diagnosed cancer and the leading cause of cancer‐related death in women globally. Its high morbidity and mortality, as well as its elevated tendency to metastasize to other organs, warrant the urgency to find new biomarkers for breast cancer diagnosis and treatment. The specific roles of long noncoding RNA linc‐ITGB1 on cell proliferation and metastasis in breast cancer were explored in this study. The expression of linc‐ITGB1 was significantly upregulated in both clinical breast cancer tissues and cultured breast cancer cell lines. The linc‐ITGB1 knockdown with specific short hairpin RNA (shRNA) decreased cell proliferation and colony formation in vitro . Tumor growth in vivo was also inhibited by linc‐ITGB1 depletion. In addition, linc‐ITGB1 depletion caused cell accumulation in the G0/G1 phase. Breast cancer cell lines with linc‐ITGB1 depletion exhibited decreased migration and invasion abilities compared with the control cells. Furthermore, the linc‐ITGB1 knockdown decreased the expression of mesenchymal markers N‐cadherin and vimentin while increasing the expression of the epithelial marker E‐cadherin. Key cell cycle regulators Cdc25C and Cyclin B1 were also decreased by the linc‐ITGB1 knockdown. These data suggest that linc‐ITGB1 promotes breast cancer progression by inducing cell cycle arrest and interrupting the epithelial‐to‐mesenchymal transition process.