ArticleCommunications biology2022
Pre-activation of autophagy impacts response to olaparib in prostate cancer cells.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 22 citations in OpenAlex.
- SPOP-mediated nuclear ubiquitination degradation of p62/SQSTM1 contributes to HR repair.Oncogene · 2026Article
- CRISPR screen identifies autophagy inhibition (GNS561) as a PARP inhibitor (AZD5305) combination strategy in small cell lung cancer.Cancer & metabolism · 2026Article
- Nucleophagy removes cytotoxic trapped PARP1.Nature cell biology · 2026Article
- Autophagy impairs the sensitivity of Ewing sarcoma cells to PARP inhibitors.Cancer chemotherapy and pharmacology · 2026Article
- PARP Inhibition in Prostate Cancer: Current Status, Resistance Mechanisms, and Clinical Challenges.Cells · 2026Review
- Integrating the hallmarks of cancer into autophagy: a perspective from underlying mechanisms to therapeutic strategies.Theranostics · 2026Review
- Novel Afro-Caribbean Prostate Cancer Model Reveals Ancestry-Specific Drug Vulnerabilities with Therapeutic Implications for Black Patients.Cancer research communications · 2025Article
- An overview of autophagy inhibition as a potential clinical strategy in cancer therapy.Molecular pharmacology · 2025Review
- LightSpot Fluorescent Conjugates as Highly Efficient Tools for Lysosomal P-gp Quantification in Olaparib-Treated Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Niraparib restricts intraperitoneal metastases of ovarian cancer by eliciting CD36-dependent ferroptosis.Redox biology · 2025Article
- Targeting autophagy promotes the antitumor effect of radiotherapy on cervical cancer cells.Cancer biology & therapy · 2024Article
- Crizotinib Enhances PARP Inhibitor Efficacy in Ovarian Cancer Cells and Xenograft Models by Inducing Autophagy.Molecular cancer research : MCR · 2024Article
- Targeting S6K/NFκB/SQSTM1/Polθ signaling to suppress radiation resistance in prostate cancer.Cancer letters · 2024Article
- Role of actin-binding proteins in prostate cancer.Frontiers in cell and developmental biology · 2024Review
- To eat or not to eat: a critical review on the role of autophagy in prostate carcinogenesis and prostate cancer therapeutics.Frontiers in pharmacology · 2024Review
- Micelle encapsulation zinc-doped copper oxide nanocomposites reverse Olaparib resistance in ovarian cancer by disrupting homologous recombination repair.Bioengineering & translational medicine · 2023Article
- Pixelated Microfluidics for Drug Screening on Tumour Spheroids and Ex Vivo Microdissected Tumour Explants.Cancers · 2023Article
- Establishment of a lysosome-related prognostic signature in breast cancer to predict immune infiltration and therapy response.Frontiers in oncology · 2023Article
- A genome-wide CRISPR-Cas9 knockout screen identifies novel PARP inhibitor resistance genes in prostate cancer.Oncogene · 2022Article
- Development of Olaparib-Resistance Prostate Cancer Cell Lines to Identify Mechanisms Associated with Acquired Resistance.Cancers · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly (ADP-ribose) polymerase 1 (PARP1) plays an essential role in DNA repair and is targeted by anticancer therapies using PARP inhibitors (PARPi) such as olaparib. PARPi treatment in prostate cancer (PC) is currently used as a monotherapy or in combination with standard therapies (hormonotherapy) in clinical trials for patients with DNA damage response mutation. Unfortunately, 20% of these patients did not respond to this new treatment. This resistance mechanism in PC is still not well understood. Here, we report that autophagy affects differently the response of PC cell lines to olaparib depending on its activation status. Pre-activation of autophagy before olaparib resulted in an increase of DNA repair activity by homologous recombination (HR) to repair double-strand breaks induced by olaparib and enhanced cell proliferation. When autophagy was activated after olaparib treatment, or completely inhibited, PC cells demonstrated an increased sensitivity to this PARPi. This autophagy-mediated resistance is, in part, regulated by the nuclear localization of sequestrosome 1 (SQSTM1/p62). Decrease of SQSTM1/p62 nuclear localization due to autophagy pre-activation leads to an increase of filamin A (FLNA) protein expression and BRCA1/Rad51 recruitment involved in the HR pathway. Our results reveal that autophagy basal levels may in part determine amenability to PARPi treatment.
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