Evidence map›Paper›PMID 40665712›Full record

ArticleCancer research and treatment2026

Keratin 6A Overexpression in the Lymphovascular Invasion-Associated Tumor Subgroup Promotes Progression of Triple-Negative Breast Cancer.

Wei Luo, Yiping Zou, Yantao Jiang, Xi Ma, Shuyue Guo, Yao Wang, Yuxiao Liu, Linyue Hai, Wenbin Jia, Wenbo Liu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer research and treatment, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

14 authors.

Wei Luo *Department of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yiping Zou *Pancreas Center, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, State Key Laboratory of Druggability Evaluation and Systematic Translational Medicine, Tianjin Key Laboratory of Digestive Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yantao Jiang *Department of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Xi MaPancreas Center, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, State Key Laboratory of Druggability Evaluation and Systematic Translational Medicine, Tianjin Key Laboratory of Digestive Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Shuyue GuoDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yao WangDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yuxiao LiuPancreas Center, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, State Key Laboratory of Druggability Evaluation and Systematic Translational Medicine, Tianjin Key Laboratory of Digestive Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Linyue HaiThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Wenbin JiaThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Wenbo LiuThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Ran MengThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Xuchen CaoThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Xianhui RuanDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China. xhruan1990@tmu.edu.cn.
Yue YuThe First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China. yuyue@tmu.edu.cn.

Funding

National Natural Science Foundation of China 82103386National Natural Science Foundation of China 82172835
6 · The paper itself

Abstract

purposeLymphovascular invasion (LVI) is a strong predictor of poor prognosis in triple-negative breast cancer (TNBC), yet its molecular basis remains unclear. This study investigates epithelial regulators associated with LVI and their functional roles in TNBC progression. MATERIALS AND

methodsWe utilized single-cell sequencing data to further characterize epithelial cell populations in TNBC, identifying dominant epithelial clusters in LVI-positive TNBC tissues. The prognostic significance of dominant epithelial marker genes was explored through transcriptomic analysis and immunohistochemical staining of patient samples from our center. Additionally, the effects of the marker gene on TNBC cell invasion and metastasis were validated in vitro and in vivo.

resultsSingle-cell data analysis revealed nine distinct epithelial cell clusters within TNBC tissues. Among these, cluster 4 was identified as the dominant epithelial subpopulation in LVI-positive TNBC, marked by the prognostic gene KRT6A. Multiple datasets confirmed KRT6A as a crucial prognostic marker in TNBC. Functional assays, including Cell Counting Kit-8, wound healing, transwell assays, and animal experiments, demonstrated that KRT6A knockdown significantly impaired the proliferation, invasion, and metastatic potential of TNBC cells. Mechanistically, KRT6A promoted epithelial-mesenchymal transition (EMT) and activated Wnt/β-catenin signaling by stabilizing β-catenin through glycogen synthase kinase-3β phosphorylation.

conclusionKRT6A promotes EMT and metastasis in TNBC via Wnt/β-catenin signaling, contributing to LVI and chemoresistance. It may serve as a prognostic biomarker and therapeutic target in TNBC.

Indexed as

Biomarkers, TumorKeratin-6Triple Negative Breast NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansLymphatic MetastasisMiceNeoplasm InvasivenessPrognosisBiomarkers, TumorKeratin-6KRT6A protein, humanEpithelial-mesenchymal transitionKeratin-6Lymphovascular invasionSingle-cell sequencingTriple negative breast neoplasms

Identifiers

PMID40665712
PMCPMC13382563

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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.