Role of the RNA-binding protein La in cancer pathobiology

RNA Biol. 2021 Feb;18(2):218-236. doi: 10.1080/15476286.2020.1792677. Epub 2020 Jul 20.

Abstract

RNA-binding proteins are important regulators of RNA metabolism and are of critical importance in all steps of the gene expression cascade. The role of aberrantly expressed RBPs in human disease is an exciting research field and the potential application of RBPs as a therapeutic target or a diagnostic marker represents a fast-growing area of research.Aberrant overexpression of the human RNA-binding protein La has been found in various cancer entities including lung, cervical, head and neck, and chronic myelogenous leukaemia. Cancer-associated La protein supports tumour-promoting processes such as proliferation, mobility, invasiveness and tumour growth. Moreover, the La protein maintains the survival of cancer cells by supporting an anti-apoptotic state that may cause resistance to chemotherapeutic therapy.The human La protein represents a multifunctional post-translationally modified RNA-binding protein with RNA chaperone activity that promotes processing of non-coding precursor RNAs but also stimulates the translation of selective messenger RNAs encoding tumour-promoting and anti-apoptotic factors. In our model, La facilitates the expression of those factors and helps cancer cells to cope with cellular stress. In contrast to oncogenes, able to initiate tumorigenesis, we postulate that the aberrantly elevated expression of the human La protein contributes to the non-oncogenic addiction of cancer cells. In this review, we summarize the current understanding about the implications of the RNA-binding protein La in cancer progression and therapeutic resistance. The concept of exploiting the RBP La as a cancer drug target will be discussed.

Keywords: Bcl2; BiP; CCND1; IRES; LARP; La autoantigen; La protein; La-related proteins; La/SSB; Laminin B1; Mdm2; PTM; RBP; RNA-binding; SUMO; TOP mRNAs; XIAP; anti-apoptotic; cancer; cyclin D1; invasion; non-oncogenic addiction; posttranslational modification; proliferation; translation; tumour-promoting.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Biomarkers, Tumor
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism
  • Disease Models, Animal
  • Disease Susceptibility*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Molecular Targeted Therapy
  • Neoplasms / drug therapy
  • Neoplasms / etiology*
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Phosphoproteins / antagonists & inhibitors
  • Phosphoproteins / genetics*
  • Phosphoproteins / metabolism*
  • Protein Binding
  • Protein Processing, Post-Translational
  • RNA / genetics
  • RNA / metabolism
  • RNA Processing, Post-Transcriptional
  • RNA, Transfer / genetics
  • RNA, Transfer / metabolism
  • RNA-Binding Proteins / antagonists & inhibitors
  • RNA-Binding Proteins / genetics*
  • RNA-Binding Proteins / metabolism*
  • Ribonucleoproteins / antagonists & inhibitors
  • Ribonucleoproteins / genetics
  • Ribonucleoproteins / metabolism

Substances

  • Biomarkers, Tumor
  • La protein, human
  • Phosphoproteins
  • RNA-Binding Proteins
  • Ribonucleoproteins
  • RNA
  • RNA, Transfer

Grants and funding

This work was supported by the German Research Foundation [SFB 960, B14 to T.H. and G.S.].