ArticleOncogene2022
MARK2 regulates chemotherapeutic responses through class IIa HDAC-YAP axis in pancreatic cancer.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Biofabrication and artificial intelligence strategies for investigating solid- and fluid-pressure mechanobiology in pancreatic ductal adenocarcinoma.Cancer metastasis reviews · 2026Review
- Comprehensive profiling of clinically approved kinase inhibitors reveals mutation-specific inhibitors and opportunities for drug repurposing.Nature biotechnology · 2026Article
- EGFR-19del nuclear translocation increases HDAC7 expression inhibiting the Hippo pathway and exacerbating TKI resistance in lung adenocarcinoma.Theranostics · 2026Article
- Tumor organoids in cancer medicine: from model systems to natural compound screening.Pharmaceutical biology · 2025Review
- Insights on the differences between two‑ and three‑dimensional culture systems in tumor models (Review).International journal of molecular medicine · 2025Review
- Advances in pancreatic cancer epigenetics: From the mechanism to the clinic.World journal of gastrointestinal oncology · 2025Review
- The perspective of targeting cancer cell metabolism: combination therapy approaches.Molecular biology reports · 2025Review
- HDAC4/MybL1/YAP novel signaling axis is required for pancreatic cancer metastasis to the liver.International journal of biological sciences · 2025Article
- MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer.Cancer discovery · 2024Article
- Role of MARK2 in the nervous system and cancer.Cancer gene therapy · 2024Review
- Emerging therapeutic strategies in cancer therapy by HDAC inhibition as the chemotherapeutic potent and epigenetic regulator.Medical oncology (Northwood, London, England) · 2024Review
- HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Methionine restriction and cancer treatment: a systems biology study of yeast to investigate the possible key players.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- HDAC-an important target for improving tumor radiotherapy resistance.Frontiers in oncology · 2023Review
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Despite paclitaxel's wide use in cancer treatment, patient response rate is still low and drug resistance is a major clinical obstacle. Through a Phos-tag-based kinome-wide screen, we identified MARK2 as a critical regulator for paclitaxel chemosensitivity in PDAC. We show that MARK2 is phosphorylated by CDK1 in response to antitubulin chemotherapeutics and in unperturbed mitosis. Phosphorylation is essential for MARK2 in regulating mitotic progression and paclitaxel cytotoxicity in PDAC cells. Mechanistically, our findings also suggest that MARK2 controls paclitaxel chemosensitivity by regulating class IIa HDACs. MARK2 directly phosphorylates HDAC4 specifically during antitubulin treatment. Phosphorylated HDAC4 promotes YAP activation and controls expression of YAP target genes induced by paclitaxel. Importantly, combination of HDAC inhibition and paclitaxel overcomes chemoresistance in organoid culture and preclinical PDAC animal models. The expression levels of MARK2, HDACs, and YAP are upregulated and positively correlated in PDAC patients. Inhibition of MARK2 or class IIa HDACs potentiates paclitaxel cytotoxicity by inducing mitotic abnormalities in PDAC cells. Together, our findings identify the MARK2-HDAC axis as a druggable target for overcoming chemoresistance in PDAC.
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