OncoTargets and Therapy (Sep 2019)

MicroRNA-155-3p promotes breast cancer progression through down-regulating CADM1

  • Zhang G,
  • Zhong L,
  • Luo H,
  • Wang S

Journal volume & issue
Vol. Volume 12
pp. 7993 – 8002

Abstract

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Guochao Zhang, Lele Zhong, Hao Luo, Shibing Wang Department of Breast and Thyroid Surgery, Affiliated Jining No. 1 People’s Hospital of Jining Medical University, Jining Medical University, Jining, Shandong 272011, People’s Republic of ChinaCorrespondence: Shibing WangDepartment of Breast and Thyroid Surgery, Jining No. 1 People’s Hospital, Jining Medical University. No. 6 Jiankang Road, Jining, Shandong 272011, People’s Republic of ChinaEmail [email protected]/purpose: Cell adhesion molecule 1 (CADM1) functions as a tumor suppressor and has been identified to be frequently inactivated in breast cancer, and closely associated with patients’ poor prognosis and advanced TNM stage. However, the mechanisms underlying CADM1 in breast cancer progression remains incompletely clear. miR-155, a predicted modulator of CADM1 was reported to be overexpressed in breast cancer, and its high expression level was closely related to the malignant progression of breast cancer. The present study aimed to explore whether miR-155-3p could modulate CADM1 expression and then involved in the progression of breast cancer.Methods: The expression patterns of miR-155-3p in breast cancer tissues and cell lines were determined by RT-PCR technology. The relationship between CADM1 and miR-155-3p were determined by the luciferase gene reporter and Western Blot (WB) assays. Cell proliferation, apoptosis rates and tumorigenesis were determined by CCK-8, flow cytometry and in vivo xenotransplanation experiments, respectively.Results: miR-155-3p was up-regulated in breast cancer tissues and cells when compared to the adjacent normal tissues and normal breast MCF 10A cells. The mRNA and protein levels of CADM1 showed opposite expression patterns to that of miR-155-3p expression detected, and miR-155-3p could negatively regulate CADM1 expression in breast cancer MCF-7 cells. Moreover, gain-of function assay showed that overexpression of miR-155-3p promoted cell proliferation, tumorigenesis and repressed cell apoptosis, but these effects were all significantly impaired when the cells were simultaneously transfected with OE-CADM1, the overexpressing vector of CADM1.Conclusion: This study revealed that miR-155-3p could accelerate the progression of breast cancer via down-regulation of CADM1 expression.Keywords: miR-155-3p, CADM1, breast cancer

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