Loss of the FAT1 Tumor Suppressor Promotes Resistance to CDK4/6 Inhibitors via the Hippo Pathway
Open accessAbstract
Cyclin dependent kinase 4/6 (CDK4/6) inhibitors (CDK4/6i) are effective in breast cancer; however, drug resistance is frequently encountered and poorly understood. We conducted a genomic analysis of 348 estrogen receptor-positive (ER+) breast cancers treated with CDK4/6i and identified loss-of-function mutations affecting FAT1 and RB1 linked to drug resistance. FAT1 loss led to marked elevations in CDK6, the suppression of which restored sensitivity to CDK4/6i. The induction of CDK6 was mediated by the Hippo pathway with accumulation of YAP and TAZ transcription factors on the CDK6 promoter. Genomic alterations in other Hippo pathway components were also found to promote CDK4/6i resistance. These findings uncover a tumor suppressor function of Hippo signaling in ER+ breast cancer and establish FAT1 loss as a mechanism of resistance to CDK4/6i.
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Dysregulation of the Hippo-YAP/TAZ pathway is a central resistance mechanism in various tumors to multiple targeted therapies, chemotherapies, hormonal therapies, and immunotherapies.
“Emerging evidence suggests that dysregulation of the Hippo-YAP/TAZ pathway is a central resistance mechanism in various tumors to multiple targeted therapies, chemotherapies, hormonal therapies, and immunotherapies (23–27).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [25]
The Results section ('FAT1 regulates CDK6 via the Hippo pathway'; page unavailable) reports that suppressing YAP/TAZ restored sensitivity to CDK4/6 inhibitors in FAT1-loss breast cancer cells. This supports resistance to a targeted therapy in that setting, but the paper does not establish Hippo-YAP/TAZ dysregulation as a central resistance mechanism across various tumors or against chemotherapies, hormonal therapies, and immunotherapies. (LLM, conf=0.88)
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- Authors
- Li, Z., Razavi, P., Li, Q., Toy, W., Liu, B., Ping, C., Hsieh, W., Sanchez-Vega, F., Brown, D. N., Da Cruz Paula, A. F., Morris, L., Selenica, P., Eichenberger, E., Shen, R., Schultz, N., Rosen, N., Scaltriti, M., Brogi, E., Baselga, J., Reis-Filho, J. S., & Chandarlapaty, S.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Weill Cornell Medicine (US)
- Corresponding author
- Chandarlapaty, Sarat
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2018-12
- Volume
- 34
- Issue
- 6
- Pages
- 893-905.e8
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC6294301
- OpenAlex
- W2903599006
- Cited by
- 508
- References
- 60
- Citations by year
- 2026: 41 · 2025: 70 · 2024: 73 · 2023: 75 · 2022: 75 · 2021: 84 · 2020: 62 · 2019: 28
- FWCI
- 32.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Roche
- National Cancer Institute (P30 CA08748)
- TG Therapeutics
- Breast Cancer Research Foundation
- Cancer Couch Foundation
- Breast Cancer Alliance
- Daiichi-Sankyo
- Sächsische Aufbaubank
- Novartis
- Eli Lilly and Company
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Advanced Breast Cancer Therapies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- FAT1, tumor suppressor, CDK4/6 inhibitors, drug resistance, Hippo signaling pathway, breast cancer
- MeSH terms
- Loss of Function Mutation, Hippo Signaling Pathway, Animals, Breast Neoplasms, Female, Humans, Signal Transduction, Cadherins, Mice, SCID, Mice, Inbred NOD, Protein Serine-Threonine Kinases, Mice, Knockout, Drug Resistance, Neoplasm, Xenograft Model Antitumor Assays, Tumor Suppressor Proteins, RNA Interference, Cell Line, Tumor, Tumor Burden, Protein Kinase Inhibitors, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinase 6, HEK293 Cells, MCF-7 Cells
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