ArticleBiochemical genetics2023
PLCB1 Enhances Cell Migration and Invasion in Gastric Cancer Via Regulating Actin Cytoskeletal Remodeling and Epithelial-Mesenchymal Transition.
Article in Biochemical genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 17 citations in OpenAlex.
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- Piezo1 regulates the mechanotransduction of soft matrix viscoelasticity.Nature communications · 2025Article
- Short Inverted Repeats as Mutational Hotspots and Putative Drivers of Genome Instability in Osteosarcoma.Genes · 2025Article
- Development of a prognostic risk model for predicting biochemical recurrence-free survival in patients with prostate cancer based on lysine acetylation.Translational andrology and urology · 2025Article
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- Phosphoinositide signalling in cell motility and adhesion.Nature cell biology · 2025Review
- Novel Genetic Risk Variants Associated with Oral Tongue Squamous Cell Carcinoma.Head and neck pathology · 2025Article
- Molecular mechanisms and clinicopathological characteristics of inhibin βA in thyroid cancer metastasis.International journal of molecular medicine · 2024Article
- LncRNA AC100826.1 regulated PLCB1 to promote progression in non-small cell lung cancer.Thoracic cancer · 2024Article
- Single-Cell Transcriptomic and Targeted Genomic Profiling Adjusted for Inflammation and Therapy Bias RevealPharmaceutics · 2024Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phospholipase C Beta 1 (PLCB1) regulates the abundance of PI(4,5)P2 in the plasma membrane and is implicated in various kinds of cancers. This study aimed to investigate the role and underlying mechanisms of PLCB1 in gastric cancer. Herein, it was found that PLCB1 mRNA and protein were highly expressed in gastric cancer, and high levels of PLCB1 were correlated with poor outcomes of patients with gastric cancer via the GEPIA database. Moreover, our results revealed that PLCB1 depletion inhibited gastric cancer cell proliferation, migration, and invasion. Meanwhile, PLCB1 overexpression resulted in an inverse result. Furthermore, PLCB1 mediated actin cytoskeleton rearrangement and activated the RhoA/LIMK/Cofilin pathway. Besides, PLCB1 promoted the Epithelial-Mesenchymal transition process via activating ATK signaling. In conclusion, PLCB1 promoted gastric cancer cell migratory and invasive abilities via regulating actin cytoskeleton rearrangement and Epithelial-Mesenchymal transition process. These findings imply that targeting PLCB1 may be a potential strategy to improve the prognosis of gastric cancer patients.
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