MAST1 drives cisplatin resistance in human cancers by rewiring cRaf-independent MEK activation
Open accessAbstract
Platinum-based chemotherapeutics represent a mainstay of cancer therapy, but resistance limits their curative potential. Through a kinome RNAi screen, we identified microtubule-associated serine/threonine kinase 1 (MAST1) as a main driver of cisplatin resistance in human cancers. Mechanistically, cisplatin but no other DNA-damaging agents inhibit the MAPK pathway by dissociating cRaf from MEK1, while MAST1 replaces cRaf to reactivate the MAPK pathway in a cRaf-independent manner. We show clinical evidence that expression of MAST1, both initial and cisplatin-induced, contributes to platinum resistance and worse clinical outcome. Targeting MAST1 with lestaurtinib, a recently identified MAST1 inhibitor, restores cisplatin sensitivity, leading to the synergistic attenuation of cancer cell proliferation and tumor growth in human cancer cells and patient-derived xenograft models.
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In cisplatin-resistant cells, MAST1 takes over C-RAF to re-activate the MAPK cascade.
“In this case, MAST1 took over C-RAF to re-activate MAPK cascade in cisplatin-resistant cells, and inhibition of MAST1 led to decreased MEK1 phosphorylation, explaining the effectiveness of targeting MAST1 in overcoming cisplatin resistance.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [85]
Cisplatin directly binds to cysteine 142 site of MEK1, restricting its access to C-RAF that typically phosphorylates MEK1.
“Further investigations showed that cisplatin directly binds to cysteine 142 site of MEK1, restricting its access to C-RAF that typically phosphorylates MEK1.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [85]
Knockdown of MAST1 re-sensitizes cisplatin-resistant cells to cisplatin in vitro and in vivo.
“Knockdown of MAST1 re-sensitized the resistant cells to cisplatin in vitro and in vivo.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [85]
MAST1 is a key mediator of cisplatin resistance.
“Jin et al. used multi-step kinome screens and identified MAST1, an AGC serine/threonine protein, as a key mediator of cisplatin resistance.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [85]
Inhibition of MAST1 leads to decreased MEK1 phosphorylation.
“In this case, MAST1 took over C-RAF to re-activate MAPK cascade in cisplatin-resistant cells, and inhibition of MAST1 led to decreased MEK1 phosphorylation, explaining the effectiveness of targeting MAST1 in overcoming cisplatin resistance.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [85]
MAST1 expression is specific to cisplatin rather than other similar DNA replication-interfering agents such as 5-fluorouracil.
“More interestingly, MAST1 expression was shown to be specific to cisplatin rather than other similar agents (for instance, 5-fluorouracil) that interfere with DNA replication.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [85]
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- Authors
- Jin, L., Chun, J., Pan, C., Li, D., Lin, R., Alesi, G. N., Wang, X., Kang, H.-B., Song, L., Wang, D., Zhang, G., Fan, J., Boggon, T. J., Zhou, L., Kowalski, J., Qu, C.-K., Steuer, C. E., Chen, G. Z., Saba, N. F., Boise, L. H., Owonikoko, T. K., Khuri, F. R., Magliocca, K. R., Shin, D. M., Lonial, S., & Kang, S.
- Affiliations
- Emory University (US)
- Morehouse School of Medicine (US)
- Yale University (US)
- Fudan University (CN)
- Corresponding author
- Kang, Sumin
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2018-08
- Volume
- 34
- Issue
- 2
- Pages
- 315-330.e7
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC6092215
- OpenAlex
- W2883776565
- Cited by
- 132
- References
- 42
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 28 · 2023: 27 · 2022: 22 · 2021: 19 · 2020: 10 · 2019: 8 · 2018: 3
- FWCI
- 3.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Winship Cancer Institute (IRG-17-181-04, P30CA138292)
- American Cancer Society
- U.S. Department of Defense (W81XWH-17-1-0186)
- National Institutes of Health (R01 CA175316, R01 CA207768, F31 CA183365)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Health Sciences › Medicine › Oncology › Metal complexes synthesis and properties
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- cisplatin resistance, MAPK signaling, lestaurtinib, platinum-based chemotherapy, DNA-damaging agents, patient-derived xenografts, tumor cell proliferation
- MeSH terms
- Animals, Antineoplastic Agents, Cisplatin, Enzyme Activation, Female, Humans, Microtubule-Associated Proteins, Protein Serine-Threonine Kinases, Drug Resistance, Neoplasm, Proto-Oncogene Proteins c-raf, Cell Line, Tumor, MAP Kinase Kinase 1, Mice
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