Evidence map›Paper›PMID 30319275›Full record

ArticleOncoTargets and therapy2018

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

Xia Cao, Guo-Zhao He

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  4. Review
  5. Tight junction disruptionWorld journal of clinical oncology · 2025
    Article
  6. Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025
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  7. Review
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  9. Downregulation ofTranslational cancer research · 2023
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. CLDN6: From Traditional Barrier Function to Emerging Roles in Cancers.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Claudin-6 is a single prognostic marker and functions as a tumor-promoting gene in a subgroup of intestinal type gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2020
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Xia CaoDepartment of Gynaecology, Danyang People's Hospital of Jiangsu Province, Danyang 212300, Jiangsu Province, China, hgz678@163.com.
Guo-Zhao HeDepartment of Gynaecology, Danyang People's Hospital of Jiangsu Province, Danyang 212300, Jiangsu Province, China, hgz678@163.com.
Government of Jiangsu Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

CLDN6endometrial carcinomainvasionknockdownPI3K/AKT pathwayprognosticproliferation

Identifiers

PMID30319275
PMCPMC6171518
OpenAlexW2894315674

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.