ArticleCancer management and research2019
The Cytoplasmic Expression Of CLDN12 Predicts An Unfavorable Prognosis And Promotes Proliferation And Migration Of Osteosarcoma.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- The claudin family characteristics in pan-cancer and the role of claudin12 in the malignant progression of lung adenocarcinoma.Scientific reports · 2025Article
- The research trends and hotspots of claudins in the field of cancer.Cell adhesion & migration · 2025Review
- Tight junctional protein family, Claudins in cancer and cancer metastasis.Frontiers in oncology · 2025Review
- Claudin-12: guardian of the tissue barrier or friend of tumor cells.Tissue barriers · 2025Review
- The Expression of the Claudin Family of Proteins in Colorectal Cancer.Biomolecules · 2024Review
- Expression and Targeted Application of Claudins Family in Hepatobiliary and Pancreatic Diseases.Journal of hepatocellular carcinoma · 2024Review
- Expression patterns of claudins in cancer.Heliyon · 2023Review
- Claudin and pancreatic cancer.Frontiers in oncology · 2023Review
- Article
- Tight Junction Protein Claudin-12 Is Involved in Cell Migration during Metastasis.Biomolecules · 2021Article
- Development of a Machine Learning-Based Autophagy-Related lncRNA Signature to Improve Prognosis Prediction in Osteosarcoma Patients.Frontiers in molecular biosciences · 2021Article
- Identification of a 7-mRNA signature as a prognostic biomarker in pediatric osteosarcoma.Translational cancer research · 2020Article
- Pan-Cancer Analysis of CLDN3 and Its Contribution to 5-FU Resistance in Colorectal Cancer.IET systems biologyArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo date, the impact and potential molecular mechanisms of CLDN12 and its association with malignancy in osteosarcoma have not been determined. MATERIALS AND
methodsIn the present study, the expression profiles of CLDN12 in osteosarcoma cell lines and tissues were explored by immunohistochemistry. A fetal osteoblast cell line was transfected with a eukaryotic expression plasmid, and endogenous CLDN12 in osteosarcoma cells were silenced through an RNA interference (RNAi) method. These transfections were verified, and the activation state of Thr308 site in protein kinase B (Akt) was explored by Western blotting. Moreover, the malignant phenotype of osteosarcoma cells was evaluated by cell counting kit-8 (CCK-8), colony formation, Transwell, and wound-healing assays. Furthermore, osteoblast cells were treated with the phosphatidylinositol-3-kinase (PI3K) inhibitor LY294002 to determine the impact of the PI3K/Akt signaling pathway on cell migration ability.
resultsThe results revealed that CLDN12 was overexpressed and localized in the cytoplasm of osteosarcoma cells, and its overexpression was associated with an unfavorable prognosis, irrespective of tumor node metastasis stage. In addition, the knockdown of CLDN12 in cultured osteosarcoma cells markedly attenuated cell proliferation and migration, as indicated by the Cell Counting Kit-8 assay, colony formation assay, scratch wound healing assay and Transwell migration assay. The results also demonstrated that the overexpression of CLDN12 increased the activation of Thr308 site in Akt in fetal osteoblast cells, and the PI3K inhibitor LY294002 partially decreased CLDN12-promoted proliferation and metastasis.
conclusionIn conclusion, the results of the present study indicated that CLDN12 promoted cell proliferation and migration through the PI3K/Akt signaling pathway in osteosarcoma cells, suggesting that CLDN12 may be a potential agent in the treatment of patients with osteosarcoma.
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