Long non-coding RNA SDPR-AS affects the development of non-small cell lung cancer by regulating SDPR through p38 MAPK/ERK signals

Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):3172-3179. doi: 10.1080/21691401.2019.1642904.

Abstract

We aimed to determine the roles and possible mechanism of long non-coding RNA SDPR-AS in the processes of non-small cell lung cancer (NSCLC). The expressions of SDPR-AS and SDPR in different subtypes of lung cancer (AC, SCC, LCC and SCLC) tissues and cells were determined. Three NSCLC cells were infused with pcDNA-SDPR-AS, pcDNA3.1, sh-SDPR-AS, sh-NC, si-SDPR and si-NC. The effects of SDPR-AS dysregulation on cell behaviors (including cell viability, colony forming ability, migration, invasion and apoptosis) were assessed. Moreover, the combined effects of SDPR-AS overexpression and SDPR-AS knockdown on H522 cell behaviors and the levels of p-p38 and p-ERK were investigated. SDPR-AS was lowly expressed in NSCLC tissues and cells, but had no changes in SCLC tissues and cells. Down-regulation of SDPR-AS enhanced the proliferation, migration and invasion and inhibited apoptosis of NSCLC cells (H522, H661 and H520). Overexpression of SDPR-AS exhibited opposite effects. Moreover, SDPR was positively regulated by SDPR-AS and effects of SDPR-AS on the cell biological processes of NSCLC cells were through regulation of SDPR. Besides, the levels of p-p38 and p-ERK were significantly decreased after SDPR-AS overexpression, which were dramatically changeover by SDPR knockdownsimultaneously. Our findings indicate that SDPR-AS was lowly expressed in NSCLC cells and down-regulation of SDPR-AS may promote the malignant behaviors of NSCLC cells possible through regulating SDPR expression and involving in p38 MAPK/ERK signaling pathway. SDPR-AS may serve as a prospective target for NSCLC diagnosis and therapy.

Keywords: Non-small cell lung cancer; SDPR; long non-coding RNA SDPR-AS; p38 MAPK/ERK signaling pathway.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Apoptosis / genetics
  • Carcinogenesis / genetics*
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / pathology*
  • MAP Kinase Signaling System / genetics*
  • Male
  • Middle Aged
  • Neoplasm Invasiveness / genetics
  • Phosphate-Binding Proteins / genetics*
  • RNA, Antisense / genetics*
  • RNA, Long Noncoding / genetics*
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • CAVIN2 protein, human
  • Phosphate-Binding Proteins
  • RNA, Antisense
  • RNA, Long Noncoding
  • Extracellular Signal-Regulated MAP Kinases
  • p38 Mitogen-Activated Protein Kinases