Introduction of long non-coding RNAs to regulate autophagy-associated therapy resistance in cancer

Mol Biol Rep. 2022 Nov;49(11):10761-10773. doi: 10.1007/s11033-022-07669-7. Epub 2022 Jul 9.

Abstract

Autophagy is a lysosomal degradation pathway that depends on various evolutionarily conserved autophagy-related genes (ATGs). Dysregulation of autophagy plays an important role in the occurrence and development of cancer. Chemotherapy, targeted therapy, radiotherapy, and immunotherapy are important treatment options for cancer, which can significantly improve the survival rate of cancer patients. However, the occurrence of therapy resistance results in therapeutic failure and poor prognosis of cancer. Accumulating studies have found that long non-coding RNAs (lncRNAs) are well known as crucial regulators to control autophagy through regulating ATGs and autophagy-associated signaling pathways, including the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway, ultimately mediating chemoresistance and radioresistance. Taken together, this review systematically summarizes and elucidates the pivotal role of lncRNAs in cancer chemoresistance and radioresistance via regulating autophagy. Understanding the specific mechanism of which may provide autophagy-related therapeutic targets for cancer in the future.

Keywords: Autophagy; Cancer therapy resistance; Long non-coding RNA (lncRNA).

Publication types

  • Review

MeSH terms

  • Autophagy / genetics
  • Humans
  • Neoplasms* / drug therapy
  • Neoplasms* / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • RNA, Long Noncoding
  • Phosphatidylinositol 3-Kinases
  • TOR Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt