ArticleOncogene2020
Nuclear DLC1 exerts oncogenic function through association with FOXK1 for cooperative activation of MMP9 expression in melanoma.
Article in Oncogene, 2020. 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, 25 citations in OpenAlex.
- Automated in situ microfluidic Random-seq for robust single-nucleus and spatial total RNA profiling of diverse FFPE specimens.Nature communications · 2026Article
- FOXK1: a multifaceted regulator in metabolic reprogramming and disease progression.Biology direct · 2026Review
- Towards a transcriptomic biomarker for the classification of melanocytic neoplasms.PLoS genetics · 2025Article
- Determination of trunk neural crest cell fate and susceptibility to splicing perturbation by the DLC1-SF3B1-PHF5A splicing complex.Nature communications · 2025Article
- Article
- Identification and characterization of intermediate states in mammalian neural crest cell epithelial to mesenchymal transition and delamination.bioRxiv : the preprint server for biology · 2024Article
- The oncogenic miR-429 promotes triple-negative breast cancer progression by degrading DLC1.Aging · 2023Article
- Article
- Proteasomal turnover of the RhoGAP tumor suppressor DLC1 is regulated by HECTD1 and USP7.Scientific reports · 2022Article
- Development of a novel autophagy-related gene prognostic signature for gastric cancer.Translational cancer research · 2021Article
- An autophagy-related prognostic signature associated with immune microenvironment features of uveal melanoma.Bioscience reports · 2021Article
- A regularized functional regression model enabling transcriptome-wide dosage-dependent association study of cancer drug response.PLoS computational biology · 2021Article
- Foxk1 regulates cancer progression.Annals of translational medicine · 2020Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A Rho GTPase-activating protein (RhoGAP), deleted in liver cancer 1 (DLC1), is known to function as a tumor suppressor in various cancer types; however, whether DLC1 is a tumor-suppressor gene or an oncogene in melanoma remains to be clarified. Here we revealed that high DLC1 expression was detected in most of the melanoma tissues where it was localized in both the nuclei and the cytoplasm. Functional studies unveiled that DLC1 was both required and sufficient for melanoma growth and metastasis. These tumorigenic events were mediated by nuclear-localized DLC1 in a RhoGAP-independent manner. Mechanistically, mass spectrometry analysis identified a DLC1-associated protein, FOXK1 transcription factor, which mediated oncogenic events in melanoma by translocating and retaining DLC1 into the nucleus. RNA-sequencing profiling studies further revealed MMP9 as a direct target of FOXK1 through DLC1-regulated promoter occupancy for cooperative activation of MMP9 expression to promote melanoma invasion and metastasis. Concerted action of DLC1-FOXK1 in MMP9 gene regulation was further supported by their highly correlated expression in melanoma patients' samples and cell lines. Together, our results not only unravel a mechanism by which nuclear DLC1 functions as an oncogene in melanoma but also suggest an unexpected role of RhoGAP protein in transcriptional regulation.
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