ArticleOncogene2014
ROCK has a crucial role in regulating prostate tumor growth through interaction with c-Myc.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 83 citations in OpenAlex.
- Rho GTPases in cancer resistance: mechanisms, vulnerabilities, and therapeutic opportunities.Biochemical Society transactions · 2026Review
- Dysregulation of Rho-Associated Coiled-Coil Protein Kinase1 Depletes Neural Stem Cell Pool and Impairs Hippocampal Neurogenesis After Traumatic Brain Injury.Cell proliferation · 2026Article
- G-protein-coupled receptor ADGRG1 drives a protective microglial state in Alzheimer's disease through MYC activation.Neuron · 2025Article
- Pioneering first-in-class HDAC-ROCK inhibitors as potential multitarget anticancer agents.Future medicinal chemistry · 2025Article
- Angelica gigas Nakai (Korean Dang-gui) Root Alcoholic Extracts in Health Promotion and Disease Therapy - active Phytochemicals and In Vivo Molecular Targets.Pharmaceutical research · 2025Article
- Rho/ROCK Pathway as a Therapeutic Target in Multiple Diseases.International journal of drug discovery and pharmacology · 2025Article
- Y-27632 targeting ROCK1&2 modulates cell growth, fibrosis and epithelial-mesenchymal transition in hyperplastic prostate by inhibiting β-catenin pathway.Molecular biomedicine · 2024Article
- NOP16 promotes hepatocellular carcinoma progression and triggers EMT through the Keap1-Nrf2 signaling pathway.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024Article
- Mechanism of RhoA regulating benign prostatic hyperplasia: RhoA-ROCK-β-catenin signaling axis and static & dynamic dual roles.Molecular medicine (Cambridge, Mass.) · 2023Article
- Mitotic protein kinase-driven crosstalk of machineries for mitosis and metastasis.Experimental & molecular medicine · 2022Review
- Rho-Kinase as a Target for Cancer Therapy and Its Immunotherapeutic Potential.International journal of molecular sciences · 2021Review
- High expression of miR-17-5p in tumor epithelium is a predictor for poor prognosis for prostate cancer patients.Scientific reports · 2021Article
- Review
- mRNA and miRNA Expression Analyses of theInternational journal of molecular sciences · 2021Article
- Peripubertal high-fat diet promotes c-Myc stabilization in mammary gland epithelium.Cancer science · 2020Article
- Regulation of RhoA GTPase and novel target proteins for ROCK.Small GTPases · 2020Review
- Long Noncoding RNA KCNMB2-AS1 Increases ROCK1 Expression by Sponging microRNA-374a-3p to Facilitate the Progression of Non-Small-Cell Lung Cancer.Cancer management and research · 2020Article
- Targeting the RhoGTPase/ROCK pathway for the treatment of VHL/HIF pathway-driven cancers.Small GTPases · 2020Review
- Article
- Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications.Medicines (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rho-associated kinase (ROCK) has an essential role in governing cell morphology and motility, and increased ROCK activity contributes to cancer cell invasion and metastasis. Burgeoning data suggest that ROCK is also involved in the growth regulation of tumor cells. However, thus far, the molecular mechanisms responsible for ROCK-governed tumor cell growth have not been clearly elucidated. Here we showed that inhibition of ROCK kinase activity, either by a selective ROCK inhibitor Y27632 or by specific ROCK small interfering RNA (siRNA) molecules, attenuated not only motility but also the proliferation of PC3 prostate cancer cells in vitro and in vivo. Importantly, mechanistic investigation revealed that ROCK endowed cancer cells with tumorigenic capability, mainly by targeting c-Myc. ROCK could increase the transcriptional activity of c-Myc by promoting c-Myc protein stability, and ROCK inhibition reduced c-Myc-mediated expression of mRNA targets (such as HSPC111) and microRNA targets (such as miR-17-92 cluster). We provided evidence demonstrating that ROCK1 directly interacted with and phosphorylated c-Myc, resulting in stabilization of the protein and activation of its transcriptional activity. Suppression of ROCK-c-Myc downstream molecules, such as c-Myc-regulated miR-17, also impaired tumor cell growth in vitro and in vivo. In addition, c-Myc was shown to exert a positive feedback regulation on ROCK by increasing RhoA mRNA expression. Therefore, inhibition of ROCK and its stimulated signaling might prove to be a promising strategy for restraining tumor progression in prostate cancer.
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