ArticlePloS one2016
Lowered Expression of Tumor Suppressor Candidate MYO1C Stimulates Cell Proliferation, Suppresses Cell Adhesion and Activates AKT.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- The class II myosin MYH4 safeguards genome integrity and suppresses tumor progression.The Journal of clinical investigation · 2025Article
- Actin from within - how nuclear myosins and actin regulate nuclear architecture and mechanics.Journal of cell science · 2025Review
- Positive regulation of oxidative phosphorylation by nuclear myosin 1 protects cells from metabolic reprogramming and tumorigenesis in mice.Nature communications · 2023Article
- Class I Myosins, molecular motors involved in cell migration and cancer.Cell adhesion & migration · 2022Article
- Responsible Genes for Neuronal Migration in the Chromosome 17p13.3: BeyondBrain sciences · 2021Review
- Oral vitamin D supplementation induces transcriptomic changes in rectal mucosa that are linked to anti-tumour effects.BMC medicine · 2021Article
- Clinical-grade whole-genome sequencing and 3' transcriptome analysis of colorectal cancer patients.Genome medicine · 2021Article
- Nuclear myosin 1 activates p21 gene transcription in response to DNA damage through a chromatin-based mechanism.Communications biology · 2020Article
- Basic-hydrophobic sites are localized in conserved positions inside and outside of PH domains and affect localization ofMolecular biology of the cell · 2020Article
- Article
- Calcium and Nuclear Signaling in Prostate Cancer.International journal of molecular sciences · 2018Review
- Single-walled and multi-walled carbon nanotubes induce sequence-specific epigenetic alterations in 16 HBE cells.Oncotarget · 2018Article
- Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myosin-1C (MYO1C) is a tumor suppressor candidate located in a region of recurrent losses distal to TP53. Myo1c can tightly and specifically bind to PIP2, the substrate of Phosphoinositide 3-kinase (PI3K), and to Rictor, suggesting a role for MYO1C in the PI3K pathway. This study was designed to examine MYO1C expression status in a panel of well-stratified endometrial carcinomas as well as to assess the biological significance of MYO1C as a tumor suppressor in vitro. We found a significant correlation between the tumor stage and lowered expression of MYO1C in endometrial carcinoma samples. In cell transfection experiments, we found a negative correlation between MYO1C expression and cell proliferation, and MYO1C silencing resulted in diminished cell migration and adhesion. Cells expressing excess of MYO1C had low basal level of phosphorylated protein kinase B (PKB, a.k.a. AKT) and cells with knocked down MYO1C expression showed a quicker phosphorylated AKT (pAKT) response in reaction to serum stimulation. Taken together the present study gives further evidence for tumor suppressor activity of MYO1C and suggests MYO1C mediates its tumor suppressor function through inhibition of PI3K pathway and its involvement in loss of contact inhibition.
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