4.7 Article

S-Adenosyl-l-Methionine Overcomes uL3-Mediated Drug Resistance in p53 Deleted Colon Cancer Cells

期刊

出版社

MDPI
DOI: 10.3390/ijms22010103

关键词

uL3; drug resistance; AdoMet; autophagy; apoptosis; colon cancer

资金

  1. Regione Campania-POR Campania FESR 2014/2020 Combattere la resistenza tumorale: piattaforma integrata multidisciplinare per un approccio tecnologico innovativo alle oncoterapie-Campania Oncoterapie [B61G18000470007]
  2. Fondo di ricerca di base FFABR-2017
  3. Ministero della Universita e della Ricerca (MIUR)
  4. Programme Valere 2020 (Vanvitelli per la Ricerca
  5. Universita della Campania Luigi Vanvitelli)
  6. Department of Precision Medicine, Universita della Campania Luigi Vanvitelli

向作者/读者索取更多资源

This study demonstrated that S-adenosyl-l-methionine can overcome drug resistance in colon cancer cells lacking p53 through multiple mechanisms, including cell cycle arrest, autophagy inhibition, reactive oxygen species augmentation, and apoptosis induction. The results suggest that S-adenosyl-l-methionine may hold promise as a potential agent for cancer therapy by examining p53 and uL3 profiles in tumors to improve clinical outcomes.
Purpose: In order to study novel therapeutic approaches taking advantage of natural compounds showing anticancer and anti-proliferative effects, we focused our interest on S-adenosyl-l-methionine, a naturally occurring sulfur-containing nucleoside synthesized from adenosine triphosphate and methionine by methionine adenosyltransferase, and its potential in overcoming drug resistance in colon cancer cells devoid of p53. Results: In the present study, we demonstrated that S-adenosyl-l-methionine overcomes uL3-mediated drug resistance in p53 deleted colon cancer cells. In particular, we demonstrated that S-adenosyl-l-methionine causes cell cycle arrest at the S phase; inhibits autophagy; augments reactive oxygen species; and induces apoptosis in these cancer cells. Conclusions: Results reported in this paper led us to propose S-adenosyl-l-methionine as a potential promising agent for cancer therapy by examining p53 and uL3 profiles in tumors to yield a better clinical outcomes.

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