STAT3-regulated LncRNA LINC00160 mediates cell proliferation and cell metabolism of prostate cancer cells by repressing RCAN1 expression

Mol Cell Biochem. 2022 Mar;477(3):865-875. doi: 10.1007/s11010-021-04284-1. Epub 2022 Jan 24.

Abstract

Long non-coding RNA (LncRNA) LINC00160 was reported to be associated with cancer progression and mediates drug resistance. However, the role of LINC00160 in prostate cancer remains unclear. The study sought to study the function of LINC00160 in prostate cancer. Moreover, the potential mechanism was investigated. Silence of LINC00160 inhibited proliferation and promoted the apoptosis of prostate cancer cells, retarded the glycolysis of prostate cancer cells. By acting as a transcription activator, STAT3 induced LINC00160 expression, which regulated RCAN1 transcription epigenetically via binding to EZH2. Mechanically, LINC00160 mediated prostate cell proliferation and metabolism by repressing RCAN1 expression. In summary, LINC00160 may function as the novel marker for prostate cancer diagnosis and therapy.

Keywords: EZH2; LINC00160; RCAN1; STAT3.

MeSH terms

  • Cell Proliferation*
  • DNA-Binding Proteins / biosynthesis*
  • DNA-Binding Proteins / genetics
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Male
  • Muscle Proteins / biosynthesis*
  • Muscle Proteins / genetics
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • PC-3 Cells
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / metabolism*
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism*

Substances

  • DNA-Binding Proteins
  • Muscle Proteins
  • Neoplasm Proteins
  • RCAN1 protein, human
  • RNA, Long Noncoding
  • RNA, Neoplasm
  • STAT3 Transcription Factor
  • STAT3 protein, human