PAIP1 regulates expression of immune and inflammatory response associated genes at transcript level in liver cancer cell

PeerJ. 2023 Apr 21:11:e15070. doi: 10.7717/peerj.15070. eCollection 2023.

Abstract

Poly(A) binding protein interacting protein 1 (PAIP1) is a translation regulator and also regulate the decay of mRNA. PAIP1 has also been reported to be a marker of increased invasive potential of liver cancer. However, the roles and underlying molecular mechanism of PAIP1 in liver cancer is still unclear. Here, cell viability and the gene expression profile of liver cancer line HepG2 transfected with PAIP1 siRNA was compared with cells transfected with non-targeting control siRNA. The results showed that PAIP1 knockdown inhibited cell viability, and extensively affects expression of 893 genes at transcriptional level in HepG2 cells. Gene function analysis showed that a large number of PAIP1 up-regulated genes were enriched in term of DNA-dependent transcription and the down-regulated genes were enriched in some pathways including immune response and inflammatory response. qPCR confirmed that PAIP1 knockdown positively regulated the expression of selected immune and inflammatory factor genes in HepG2 cells. Expression analysis of TCGA revealed that PAIP1 had positive correlations with two immune associated genes IL1R2 and PTAFR in liver tumor tissue. Taken together, our results demonstrated that PAIP1 was not only a translation regulator, but also a transcription regulator in liver cancer. Moreover, PAIP1 could function as a regulatory factor of immune and inflammatory genes in liver cancer. Thus, our study provides important cues for further study on the regulatory mechanism of PAIP1 in liver cancer.

Keywords: Gene expression; Immune response; Inflammatory response; Liver cancer; PAIP1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Humans
  • Liver Neoplasms* / genetics
  • Peptide Initiation Factors / metabolism
  • RNA, Messenger / genetics
  • RNA, Small Interfering
  • RNA-Binding Proteins / metabolism

Substances

  • RNA, Messenger
  • RNA, Small Interfering
  • RNA-Binding Proteins
  • Peptide Initiation Factors

Grants and funding

This work was supported by The National Natural Science Foundation of China (No. 81860438) and the Shenzhen Science and Technology Program (No. JCYJ20210324121012034). There was no additional external funding received for this study. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.