ArticleClinical cancer research : an official journal of the American Association for Cancer Research2023
Quiescent Ovarian Cancer Cells Secrete Follistatin to Induce Chemotherapy Resistance in Surrounding Cells in Response to Chemotherapy.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Targeting HDAC and proteostasis to eradicate quiescent cancer cells.Cancer gene therapy · 2026Article
- Identification of the MRTFA/SRF pathway as a critical regulator of quiescence and chemotherapy resistance in cancer.Cancer letters · 2026Article
- NFATc4 Promotes Lung Adenocarcinoma Progression via the CCNB1/CDK1 Pathway and Is a Potential Prognostic Biomarker.Cancer science · 2025Article
- Role of the NuRD complex and altered proteostasis in cancer cell quiescence.bioRxiv : the preprint server for biology · 2025Article
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.Molecular metabolism · 2024Article
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.bioRxiv : the preprint server for biology · 2024Article
- The Reign of Follistatin in Tumors and Their Microenvironment: Implications for Drug Resistance.Biology · 2024Review
- Exosomal noncoding RNAs in gynecological cancers: implications for therapy resistance and biomarkers.Frontiers in oncology · 2024Review
- Decoding key cell sub-populations and molecular alterations in glioblastoma at recurrence by single-cell analysis.Acta neuropathologica communications · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 3 countries.
Funding
Abstract
purposeWe recently reported that the transcription factor NFATC4, in response to chemotherapy, drives cellular quiescence to increase ovarian cancer chemoresistance. The goal of this work was to better understand the mechanisms of NFATC4-driven ovarian cancer chemoresistance. EXPERIMENTAL
designWe used RNA sequencing to identify NFATC4-mediated differential gene expression. CRISPR-Cas9 and FST (follistatin)-neutralizing antibodies were used to assess impact of loss of FST function on cell proliferation and chemoresistance. ELISA was used to quantify FST induction in patient samples and in vitro in response to chemotherapy.
resultsWe found that NFATC4 upregulates FST mRNA and protein expression predominantly in quiescent cells and FST is further upregulated following chemotherapy treatment. FST acts in at least a paracrine manner to induce a p-ATF2-dependent quiescent phenotype and chemoresistance in non-quiescent cells. Consistent with this, CRISPR knockout (KO) of FST in ovarian cancer cells or antibody-mediated neutralization of FST sensitizes ovarian cancer cells to chemotherapy treatment. Similarly, CRISPR KO of FST in tumors increased chemotherapy-mediated tumor eradication in an otherwise chemotherapy-resistant tumor model. Suggesting a role for FST in chemoresistance in patients, FST protein in the abdominal fluid of patients with ovarian cancer significantly increases within 24 hours of chemotherapy exposure. FST levels decline to baseline levels in patients no longer receiving chemotherapy with no evidence of disease. Furthermore, elevated FST expression in patient tumors is correlated with poor progression-free, post-progression-free, and overall survival.
conclusionsFST is a novel therapeutic target to improve ovarian cancer response to chemotherapy and potentially reduce recurrence rates.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.