Kaohsiung Journal of Medical Sciences (Aug 2020)

Retracted: Protective effect of hsa‐miR‐570‐3p targeting CD274 on triple negative breast cancer by blocking PI3K/AKT/mTOR signaling pathway

  • Li‐Li Wang,
  • Wei‐Wei Huang,
  • Jing Huang,
  • Rong‐Fang Huang,
  • Na‐Ni Li,
  • Yi Hong,
  • Mu‐Lan Chen,
  • Fan Wu,
  • Jian Liu

DOI
https://doi.org/10.1002/kjm2.12212
Journal volume & issue
Vol. 36, no. 8
pp. 581 – 591

Abstract

Read online

Abstract To find out the role of hsa‐miR‐570‐3p targeting CD274 in triple negative breast cancer (TNBC) via PI3K/AKT/mTOR signaling pathway. Hsa‐miR‐570‐3p and CD274 expressions in 175 TNBC patients were detected by qRT‐PCR and immunohistochemistry respectively. The human TNBC cell lines (MDA‐MB‐468 and MDA‐MB‐231) were used to verify the targeting relationship between hsa‐miR‐570‐3p and CD274 via dual‐luciferase reporter gene assay. Then, MDA‐MB‐468 and MDA‐MB‐231 cells were divided into Blank, miR‐NC, miR‐570‐3p mimics, NC siRNA, CD274 siRNA, and miR‐570‐3p inhibitors + CD274 siRNA groups. Next, the biological activities of cells were detected by MTT, Cell‐Light EdU, Annexin‐V‐FITC/PI, wound healing and Transwell invasion assays. Western blotting was conducted to detect protein expressions.MiR‐570‐3p expression was lower in tumor tissues than that in adjacent normal tissues, which was more obvious in CD274‐positive TNBC patients, which targeted CD274 in TNBC cell lines. MiR‐570‐3p inhibited cell proliferation, invasion and migration, but induced cell apoptosis accompanying the upregulation of apoptotic proteins and downregulation of anti‐apoptotic protein. CD274 siRNA had the similar results of miR‐570‐3p mimics, which could be reversed by miR‐570‐3p inhibitors. Besides, both miR‐570‐3p mimics and CD274 siRNA blocked PI3K/AKT/mTOR signaling pathway in TNBC cell lines. Hsa‐miR‐570‐3p was downregulated and CD274 was upregulated in TNBC patients. Besides, hsa‐miR‐570‐3p targeted CD274 to inhibit cell proliferation, invasion, migration, and induce cell apoptosis, which may be related to the suppression of PI3K/AKT/mTOR pathway.

Keywords