ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2014
Deregulation of the cell polarity protein Lethal giant larvae 2 (Lgl2) correlates with gastric cancer progression.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 13 citations in OpenAlex.
- Ubiquitination-Dependent LLGL2 Degradation Drives Colorectal Cancer Progression via THBS3 mRNA Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Assessment of candidate high-grade serous ovarian carcinoma predisposition genes through integrated germline and tumour sequencing.NPJ genomic medicine · 2025Article
- SOX2 inhibits LLGL2 polarity protein in esophageal squamous cell carcinoma via miRNA-142-3p.Cancer biology & therapy · 2022Article
- [MiR-665 Promotes the Biological Behavior of Small Cell Lung Cancer by Targeting LLGL1].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020Article
- Loss ofCanadian journal of gastroenterology & hepatology · 2019Article
- Inhibition of the miR-192/215-Rab11-FIP2 axis suppresses human gastric cancer progression.Cell death & disease · 2018Article
- Article
- Spatiotemporal phosphoregulation of Lgl: Finding meaning in multiple on/off buttons.Bioarchitecture · 2016Article
- Expression of polarity genes in human cancer.Cancer informatics · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe investigated the roles of Lethal giant larvae 2 (Lgl2), an epithelial cell polarity protein, during gastric carcinogenesis and gastric cancer (GC) progression and evaluated the correlation of Lgl2 with epithelial-mesenchymal transition (EMT) markers.
methodsLgl2 protein and mRNA expression were determined by immunohistochemistry and mRNA in situ hybridization in a large series of GC and preneoplastic lesions. Additionally, expression of 7 EMT markers was examined by immunohistochemistry.
resultsLoss of membrane Lgl2 staining in GC was observed in 347 of 409 GCs. Lgl2 loss was associated with diffuse histological type (P < 0.001), advanced stage (P = 0.021), and worse prognosis (P = 0.047). Furthermore, Lgl2 loss correlated with reduced E-cadherin expression (P < 0.01) and increased expression of vimentin (P < 0.01). Combined analysis of Lgl2 and the EMT markers, S100A4 and MMP2, improved predictions of patient outcomes. During gastric carcinogenesis, membrane expression of Lgl2 was progressively lost in 4 % of normal mucosa, 75 % of intestinal metaplasia, 58 % of gastric dysplasia, 69 % of intestinal type GC, and 96 % of diffuse type GC.
conclusionsOur results suggest that Lgl2 loss occurs at an early stage of gastric carcinogenesis and contributes to GC progression.
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