Abstract
Olaparib, a PARP inhibitor, is effective against various cancers, including prostate cancer. However, resistance to olaparib poses a significant challenge. This study uncovers that mitochondrial alterations and PINK1 gene overexpression contribute to this resistance in prostate cancer cells. Enhanced mitochondrial functionality and increased PINK1 expression in olaparib-resistant cells underscore the importance of targeting mitochondrial dynamics and PINK1 to develop more effective treatments for overcoming olaparib resistance in prostate cancer.
©2024 The Authors; Published by the American Association for Cancer Research.
MeSH terms
-
Cell Line, Tumor
-
Drug Resistance, Neoplasm* / genetics
-
Humans
-
Male
-
Mitochondria* / drug effects
-
Mitochondria* / metabolism
-
Phthalazines* / pharmacology
-
Phthalazines* / therapeutic use
-
Piperazines* / pharmacology
-
Piperazines* / therapeutic use
-
Poly(ADP-ribose) Polymerase Inhibitors / pharmacology
-
Poly(ADP-ribose) Polymerase Inhibitors / therapeutic use
-
Prostatic Neoplasms* / drug therapy
-
Prostatic Neoplasms* / genetics
-
Prostatic Neoplasms* / metabolism
-
Prostatic Neoplasms* / pathology
-
Protein Kinases* / genetics
-
Protein Kinases* / metabolism
Substances
-
olaparib
-
Phthalazines
-
Piperazines
-
PTEN-induced putative kinase
-
Protein Kinases
-
Poly(ADP-ribose) Polymerase Inhibitors