Evidence map›Paper›PMID 32329414›Full record

ArticleTechnology in cancer research & treatment

KRT6A Promotes EMT and Cancer Stem Cell Transformation in Lung Adenocarcinoma.

Bin Yang, Wei Zhang, Mengmeng Zhang, Xuhong Wang, Shengzu Peng, Rongsheng Zhang

Open access · goldAbstract read
In one paragraph

Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
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  12. Distinct molecular subtypes of KRASClinical and translational medicine · 2025
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  17. Integrated analysis of single-cell and bulk RNA-sequencing identifies a metastasis-related gene signature for predicting prognosis in lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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3 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Bin YangDepartment of Thoracic Surgery (III), Shanxi Cancer Hospital, Taiyuan, People's Republic of China.
Wei ZhangDepartment of General Surgery (II), The 6th Division Hospital of Xinjiang Corps, Taiyuan, People's Republic of China.
Mengmeng ZhangDepartment of Gastrointestinal Surgery, Laboratory of Surgical Oncology, Peking University People's Hospital, Taiyuan, People's Republic of China.
Xuhong WangDepartment of Head and Neck Surgery, Shanxi Cancer Hospital, Taiyuan, People's Republic of China.
Shengzu PengDepartment of Thoracic Surgery (III), Shanxi Cancer Hospital, Taiyuan, People's Republic of China.
Rongsheng ZhangDepartment of Thoracic Surgery (III), Shanxi Cancer Hospital, Taiyuan, People's Republic of China.ORCID 0000-0001-6219-294X
Shanxi Provincial Cancer Hospital · CNPeking University · CNXinjiang Production and Construction Corps · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimKeratin 6A is a type II cytokeratin which is important in forming nail bed, filiform papillae, the epithelial lining of oral mucosa, and esophagus; recently, keratin 6A was found hyperexpressed in different types of cancer. But, the biological function of keratin 6A in lung adenocarcinoma still remains unclear. Therefore, in current study, we investigated the biological role of keratin 6A in lung adenocarcinoma.

methodsBy utilizing The Cancer Genome Atlas database, we investigated the expression profile of keratin 6A and its relationship with other clinical parameters in lung adenocarcinoma. The biological function of keratin 6A in lung adenocarcinoma was also investigated by using A549 and PC-9 lung cancer cell lines

resultsOur data indicate that, compared with normal lung tissue samples, keratin 6A was hyperexpressed in lung adenocarcinoma. Moreover, keratin 6A hyperexpression was positively correlated with lymph node positive and aggressive tumor T stage. Keratin 6A knockdown inhibited the cell proliferation, migration, and colony formation ability but not cell death in lung adenocarcinoma cells. In addition, we found keratin 6A exerted its phenotype via promoting cancer stem cells (CXCR4

conclusionIn conclusion, current study suggests that hyperexpressed keratin 6A in lung adenocarcinoma promotes lung cancer proliferation and metastasis via epithelial-mesenchymal transition and cancer stem cells transformation.

Indexed as

Epithelial-Mesenchymal TransitionAdenocarcinoma of LungApoptosisBiomarkers, TumorCell MovementCell ProliferationCell Transformation, NeoplasticHumansKeratin-6Lung NeoplasmsNeoplastic Stem CellsPrognosisTumor Cells, CulturedBiomarkers, TumorKeratin-6KRT6A protein, humancancer stem cellsEMTKRT6Alung adenocarcinomametastasis

Identifiers

PMID32329414
PMCPMC7225834
OpenAlexW3018026506

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

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.