LncRNA-135528 inhibits tumor progression by up-regulating CXCL10 through the JAK/STAT pathway

Apoptosis. 2018 Dec;23(11-12):651-666. doi: 10.1007/s10495-018-1482-7.

Abstract

Spontaneous tumor regression can be observed in many tumors, however, studies related to the altered expression of lncRNA in spontaneous glioma regression are limited, and the potential contributions of lncRNAs to spontaneous glioma regression remain unknown. To investigate the biological roles of lncRNA-135528 in spontaneous glioma regression. The cDNA fragment of lncRNA-135528 was obtained by rapid-amplification of cDNA ends (RACE) technology and cloned into the plvx-mcmv-zsgreen-puro vector. Additionally, we stably silenced or overexpressed lncRNA-135528 in G422 cells by transfecting with siRNA against lncRNA-135528 or lncRNA-135528 overexpression plasmid. Then, we examined lncRNA-135528 overexpressing and lncRNA-135528 silencing on glioma cells and its effects on CXCL10 and JAK/STAT pathways. The main findings indicated that lncRNA-135528 promoted glioma cell apoptosis, inhibited cell proliferation and arrested cell cycle progression; the up-regulation of lncRNA135528 led to significantly increased CXCL10 levels and the differential expression of mRNA associated with JAK/STAT pathway in glioma cells. lncRNA-135528 can inhibit tumor progression by up-regulating CXCL10 through the JAK/STAT pathway.

Keywords: CXCL10; Glioma; JAK/STAT pathways; LncRNA-135528; Spontaneous tumor regression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Brain Neoplasms / genetics
  • Brain Neoplasms / metabolism
  • Brain Neoplasms / pathology
  • Cell Cycle
  • Cell Line, Tumor
  • Cell Proliferation
  • Chemokine CXCL10 / genetics*
  • Gene Expression Profiling
  • Gene Silencing
  • Glioma / genetics
  • Glioma / metabolism
  • Glioma / pathology
  • Humans
  • Janus Kinases / genetics*
  • Janus Kinases / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Neoplasm Regression, Spontaneous / genetics*
  • Neoplasm Regression, Spontaneous / pathology
  • Neoplasm Regression, Spontaneous / physiopathology
  • RNA, Long Noncoding / antagonists & inhibitors
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*
  • RNA, Messenger / metabolism
  • STAT Transcription Factors / genetics*
  • STAT Transcription Factors / metabolism
  • Signal Transduction / genetics
  • Transcriptional Activation*

Substances

  • Chemokine CXCL10
  • RNA, Long Noncoding
  • RNA, Messenger
  • STAT Transcription Factors
  • Janus Kinases