CLDN6 (claudin 6)

Rendon-Huerta, EP; Torres-Martínez, AC; Montaño, Luis F.

doi:10.4267/2042/50188

Cited by 2 publications

(2 citation statements)

References 14 publications

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“… 7 – 10 CLDN6, a member of CLDN family, is located on 16p13.3 and maintains cell-cell junctions in epithelial cell sheets, and the expression of this gene is mainly observed in mouse embryonic stem cells and primitive germ cell tumors. 11 CLDN6 has been demonstrated to suppress cancer cell growth and induce cell apoptosis. 12 , 13 In a former study, CLDN6 has been demonstrated to function as a tumor suppressor in breast cancer, inhibiting the breast cancer cell growth, migration, as well as invasion through p38/mitogen-activated protein kinase (MAPK) pathway.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of CLDN6 inhibits cell proliferation and migration via PI3K/AKT/mTOR signaling pathway in endometrial carcinoma cell line HEC-1-B

Cao

2018

OTT

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BackgroudDysregulation of claudin-6 (CLDN6) expression in cancers has been widely documented. However, no study has reported a complete mechanistic understanding of CLDN6 regulation and function in endometrial carcinoma (EC) progression. In the current study, we aimed to assess the expression and biological functions of CLDN6 in EC.MethodsFirstly, the expression level of CLDN6 in EC was measured based on The Cancer Genome Atlas (TCGA) database. Then, qRT-PCR and western blotting were implemented to detect the expression levels of CLDN6 in 82 pairs of EC tissues and corresponding non-tumor tissues, as well as EC cell line HEC-1B. After knockdown of CLDN6, with the attempt to assess whether CLDN6 reduction had positive effects on the cell proliferation, clone formation, invasion and migration abilities of HLC-1Bs, cell counting kit-8 (CCK-8) assay (24, 48, 72 and 96 hours post-transfection), clone experiment, and invasion and migration assays were conducted. Through western blotting analysis, CLDN6-mediated phosphatidylinositol 3-kinase (PI3K) pathway was evaluated.ResultsBased on the data of TCGA database, clinical patients and cell line HEC-1B, CLDN6 was up-regulated in EC compared with normal. Univariate as well as multivariate COX analysis indicated that CLDN6 expression can act as an independent prognostic factor for overall survival of EC. Further, knockdown of CLDN6 significantly inhibited HEC-1B cell proliferation, suppressed the colony numbers of HEC-1-B cells, and restrained the invasive and migratory ability of HEC-1-B cells. Importantly, through western blot analysis, we found that inhibition of CLDN6 remarkably decreased p-AKT, p-PI3K, and mTOR expression level in EC HEC-1B cell line.ConclusionOur data underscore the significance of CLDN6 in EC progression, and CLDN6 is a new candidate oncogene in EC. Our findings propose that targeting CLDN6 might offer future clinical utility in EC.

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Section: Introductionmentioning

confidence: 99%

Knockdown of CLDN6 inhibits cell proliferation and migration via PI3K/AKT/mTOR signaling pathway in endometrial carcinoma cell line HEC-1-B

Cao

2018

OTT

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“…CLDN6 gene is located on 16p13.3 and its expression is mainly found in mouse embryonic stem cells, epithelial lineage cells during early development and primitive germ cell tumors such as spermatocytic seminoma, embryonal carcinoma, mature teratoma and classic seminoma ( 6 ). Its expression is very weak or absent in mouse and tumor tissue ( 7 – 9 ).…”

Section: Introductionmentioning

confidence: 99%

Bioinformatic analysis reveals potential properties of human Claudin-6 regulation and functions

Lin

Guo

et al. 2017

Oncology Reports

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Abstract. is an integral component of the tight junction proteins in polarized epithelial and endothelial cells and plays a crucial role in maintaining cell integrity. Deregulation of CLDN6 expression and distribution in tumor tissues have been widely documented and correlated with cancer progression and metastasis. However, a complete mechanistic understanding of CLDN6 regulation and function remains to be studied. Herein, we show new potential properties of CLDN6 regulation and functions from bioinformatics analysis. Using numerous algorithms to characterize the CLDN6 gene promoter elements and the CLDN6 protein structure, physio-chemical and localization properties, and its evolutionary relationships. CLDN6 is regulated by a diverse set of transcription factors (SP1, SPR, AML-1a, CdxA, CRE-BP and CREB) and associated with the levels of methylation of CpG islands in promoters. The structural properties of CLDN6 indicate that it promotes cancer cell behavior via the ASK1-p38/JNK MAPK secretory signaling pathway. In conclusion, this information from bioinformatics analysis will help future attempts to better understand CLDN6 regulation and functions.

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CLDN6 (claudin 6)

Cited by 2 publications

References 14 publications

Knockdown of CLDN6 inhibits cell proliferation and migration via PI3K/AKT/mTOR signaling pathway in endometrial carcinoma cell line HEC-1-B

Knockdown of CLDN6 inhibits cell proliferation and migration via PI3K/AKT/mTOR signaling pathway in endometrial carcinoma cell line HEC-1-B

Bioinformatic analysis reveals potential properties of human Claudin-6 regulation and functions

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