ArticleFrontiers in oncology2021
LLGL2 Increases Ca
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Collagen prolyl 4-hydroxylase subunit α member-induced head and neck squamous cell carcinoma aggressiveness is antagonized by LLGL2 via reduced expression of occludin.Acta biochimica et biophysica Sinica · 2024Article
- Gamma-aminobutyric acid for delaying type 1 diabetes mellitus: an update.Annals of pediatric endocrinology & metabolism · 2024Article
- Novel role of LLGL2 silencing in autophagy: reversing epithelial-mesenchymal transition in prostate cancer.Biological research · 2024Article
- Stroma-associated FSTL3 is a factor of calcium channel-derived tumor fibrosis.Scientific reports · 2023Article
- Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy.Biomedicines · 2022Article
- Article
- Comprehensive Analysis of SLC17A9 and Its Prognostic Value in Hepatocellular Carcinoma.Frontiers in oncology · 2022Article
- Gender dimorphism in survival of patients with lymph node metastasis of bladder cancer.Therapeutic advances in medical oncology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLethal giant larvae (Lgl), scaffolding proteins, regulate the epithelial cell apicobasal polarity in Drosophila. They play important roles in asymmetric cell division, cell migration, and progenitor cells self-renewal as tumor suppressors. One of Lgl mammalian homologues proteins, LLGL2 overexpression has been reported in ER+ breast cancer and promotes tumor proliferation through regulating leucine uptake. Nonetheless, the role of LLGL2 in hepatocellular carcinoma (HCC) is still unknown.
methodsTCGA dataset mining, qRT-PCR, Western blot along with immunohistochemistry assays were employed to explore LLGL2 expression in human HCC samples and cell lines. Moreover, the clinical value of LLGL2 was investigated in 156 HCC patients. Furthermore, the role as well as the molecular mechanism of LLGL2 in the progression of HCC was explored through a series of
resultsLLGL2 was up-regulated in HCC tissues, which was related with certain clinicopathological features including tumor number, vascular invasion as well as advanced stage. High expression of LLGL2 predicted poor prognosis after hepatectomy. LLGL2 promoted HCC cells proliferation, migration and invasion through PI3K/ATK signaling by promoting calcium ion influx.
conclusionOur study identified that LLGL2 is a tumor promoter in HCC for the first time, which could potentially be utilized as a new biomarker and a therapeutic target for HCC.
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