LINC00702-mediated DUSP1 transcription in the prevention of bladder cancer progression: Implications in cancer cell proliferation and tumor inflammatory microenvironment

Genomics. 2022 Jul;114(4):110428. doi: 10.1016/j.ygeno.2022.110428. Epub 2022 Jul 6.

Abstract

Background: Long noncoding RNAs (lncRNAs) can mediate the biological processes during tumorigenesis which may be affected by tumor associated macrophages (TAMs). Hence, we aim to identify the functionality of LINC00702 in regulation of bladder cancer cells and M2-TAMs.

Methods: After induction of M2-TAMs from THP-1 monocyte, we evaluated effects of LINC00702 on bladder cancer cells and M2-TAMs, which were validated in a xenograft tumor mouse model.

Results: Low LINC00702 expression was determined in bladder cancer tissues. LINC00702 could promote DUSP1 transcription by recruiting JUND to its promoter. Ectopic LINC00702 expression suppressed the bladder cancer cell proliferation and secretion of inflammatory cytokines by M2-TAMs through up-regulation of DUSP1. The anti-tumor activity of LINC00702 was ultimately validated in vivo.

Conclusion: LINC00702 promoted DUSP1 by recruiting JUND to inhibit the proliferation of bladder cancer cells and the secretion of inflammatory factors, thus modulating bladder cancer inflammatory microenvironment.

Keywords: Bladder cancer; Dual specificity phosphatase 1; Inflammatory microenvironment; Jund proto-oncogene; Long intergenic noncoding RNA-00702; Transcription factor; Tumor associated macrophages.

MeSH terms

  • Animals
  • Cell Proliferation
  • Dual Specificity Phosphatase 1 / genetics
  • Dual Specificity Phosphatase 1 / metabolism*
  • Humans
  • Macrophages / metabolism
  • Mice
  • RNA, Long Noncoding / metabolism*
  • Tumor Microenvironment
  • Urinary Bladder Neoplasms* / genetics
  • Urinary Bladder Neoplasms* / metabolism

Substances

  • RNA, Long Noncoding
  • DUSP1 protein, human
  • Dual Specificity Phosphatase 1