ArticleCancer letters2022
Giant obscurin regulates migration and metastasis via RhoA-dependent cytoskeletal remodeling in pancreatic cancer.
Article in Cancer letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Obscurin a localizes near the cell membrane to modulate stress fiber dynamics and cell migration.The Journal of biological chemistry · 2026Article
- Explainable multi-omics modeling for risk stratification in pancreatic ductal adenocarcinoma.Gland surgery · 2026Article
- Role of Spatial Heterogeneity in Muscle-Invasive Bladder Cancer on Overall Survival and Immunotherapy Response.Cancers · 2026Article
- Multi-Omic Analysis Identifies Key Genes Driving Testicular Fusion inInternational journal of molecular sciences · 2025Article
- Tumor-derived exosomal CCT6A serves as a matchmaker introducing chemokines to tumor-associated macrophages in pancreatic ductal adenocarcinoma.Cell death & disease · 2025Article
- Genomic Characterization of High-Grade Serous Ovarian Carcinoma Reveals Distinct Somatic Features in Black Individuals.Cancer research · 2025Article
- Loss of OBSCN expression promotes bladder cancer progression but enhances the efficacy of PD-L1 inhibitors.Cell & bioscience · 2025Article
- Selective Modulation of Osteoclast Function byToxins · 2025Article
- Genomic characteristics and prognostic correlations in Chinese multiple myeloma patients.BMC medical genomics · 2025Article
- Molecular mechanisms and clinicopathological characteristics of inhibin βA in thyroid cancer metastasis.International journal of molecular medicine · 2024Article
- Mdm2 requires Sprouty4 to regulate focal adhesion formation and metastasis independent of p53.Nature communications · 2024Article
- Comprehensive somatic mutational analysis in glioblastoma: Implications for precision medicine approaches.PloS one · 2024Article
- Septin11 promotes hepatocellular carcinoma cell motility by activating RhoA to regulate cytoskeleton and cell adhesion.Cell death & disease · 2023Article
- The Cell Biology of Metastatic Invasion in Pancreatic Cancer: Updates and Mechanistic Insights.Cancers · 2023Review
- Article
- Amino acid metabolism-based molecular classification of colon adenocarcinomaFrontiers in immunology · 2022Article
- Identification of an ergosterol derivative with anti-melanoma effect from the sponge-derived fungusFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Obscurins, encoded by the OBSCN gene, are giant cytoskeletal proteins with structural and regulatory roles. Large scale omics analyses reveal that OBSCN is highly mutated across different types of cancer, exhibiting a 5-8% mutation frequency in pancreatic cancer. Yet, the functional role of OBSCN in pancreatic cancer progression and metastasis has to be delineated. We herein show that giant obscurins are highly expressed in normal pancreatic tissues, but their levels are markedly reduced in pancreatic ductal adenocarcinomas. Silencing of giant obscurins in non-tumorigenic Human Pancreatic Ductal Epithelial (HPDE) cells and obscurin-expressing Panc5.04 pancreatic cancer cells induces an elongated, spindle-like morphology and faster cell migration via cytoskeletal remodeling. Specifically, depletion of giant obscurins downregulates RhoA activity, which in turn results in reduced focal adhesion density, increased microtubule growth rate and faster actin dynamics. Although OBSCN knockdown is not sufficient to induce de novo tumorigenesis, it potentiates tumor growth in a subcutaneous implantation model and exacerbates metastasis in a hemispleen murine model of pancreatic cancer metastasis, thereby shortening survival. Collectively, these findings reveal a critical role of giant obscurins as tumor suppressors in normal pancreatic epithelium whose loss of function induces RhoA-dependent cytoskeletal remodeling, and promotes cell migration, tumor growth and metastasis.
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