ArticleJournal of bioenergetics and biomembranes2021
Knockdown of RABL3 suppresses the proliferation and invasion of oral squamous cell carcinoma through inactivating the FAK/AKT pathway.
Article in Journal of bioenergetics and biomembranes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- RAB11A Promotes Cell Malignant Progression and Tumor Formation of Prostate Cancer via Activating FAK/AKT Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Functional and clinical characteristics of focal adhesion kinases in cancer progression.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
Rab-like 3 (RABL3) is a member of Rab family that is related with several kinds of cancers. However, the functional roles of RABL3 in oral squamous cell carcinoma (OSCC) remain largely unknown. In the current study, we examined the expression levels of RABL3 in OSCC tissues and cell lines. The results showed that RABL3 expression was markedly increased in OSCC tissues and cell lines. Knockdown of RABL3 significantly suppressed the proliferation, migration and invasion of OSCC cells. Overexpression of RABL3 exhibited opposite effects with RABL3 knockdown. In vivo assay demonstrated that knockdown of RABL3 suppressed the tumorigenesis of OSCC. Moreover, RABL3 regulated the activation of focal adhesion kinase (FAK)/protein kinase B (Akt) signaling pathway in OSCC cells. Inhibition of FAK reversed the effects of RABL3 overexpression on cell proliferation, migration and invasion of OSCC cells. In conclusion, these findings demonstrated that RABL3 acted as an oncogene in OSCC, which was attributed to the regulation of FAK/Akt pathway. Thus, RABL3 may be potential therapeutic target for the treatment of OSCC.
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