Evidence map›Paper›PMID 41250218›Full record

ArticleCancer cell international2025

Increased KCNQ3 expression in papillary thyroid cancer promotes proliferation and migration.

Qiuli Li, Muyuan Liu, Xuhong Song, Lingzhu Xie, Dongchen Liu, Ting Su, Yangzhan Xu, Gengquan Li, Bin Liang, Dongyang Huang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. 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

10 authors.

Qiuli LiDepartment of Central Laboratory, Cancer Hospital of Shantou University Medical College, Shantou, China.
Muyuan LiuDepartment of Head and Neck, Cancer Hospital of Shantou University Medical College, Shantou, China.
Xuhong SongDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High- Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, No. 22, Xinling Road, Shantou, 515041, China.
Lingzhu XieDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High- Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, No. 22, Xinling Road, Shantou, 515041, China.
Dongchen LiuDepartment of Central Laboratory, Cancer Hospital of Shantou University Medical College, Shantou, China.
Ting SuDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High- Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, No. 22, Xinling Road, Shantou, 515041, China.
Yangzhan XuDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High- Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, No. 22, Xinling Road, Shantou, 515041, China.
Gengquan LiDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High- Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, No. 22, Xinling Road, Shantou, 515041, China.
Bin LiangDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High- Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, No. 22, Xinling Road, Shantou, 515041, China. bliang@stu.edu.cn.
Dongyang HuangDepartment of Central Laboratory, Cancer Hospital of Shantou University Medical College, Shantou, China. huangdy@stu.edu.cn.

Funding

National Natural Science Foundation of China 31770876National Natural Science Foundation of China,China U23A20427
6 · The paper itself

Abstract

purposePapillary thyroid cancer (PTC), the most prevalent thyroid malignancy, is witnessing a global surge in incidence. The potassium voltage-gated channel subfamily Q member 3 (KCNQ3) is aberrantly overexpressed in PTC, yet its mechanistic contribution to oncogenesis remains unclear. Thus, we aimed to elucidate the oncogenic mechanism of KCNQ3 in PTC.

methodsWe integrated gene expression profiling interactive analysis (GEPIA), immunohistochemistry, and western blotting to assess KCNQ3 expression during PTC tumorigenesis and progression, and validated in vitro and in vivo using BALB/c nude mice. The functional roles of KCNQ3 were evaluated using wound-healing, transwell, and colony formation assays. Protein interactions were elucidated through co-immunoprecipitation, mass spectrometry (MS), and immunofluorescence, while estradiol (E

resultsKCNQ3 was upregulated in PTC and drove tumor cell proliferation and migration. Mechanistically, KCNQ3 interacted with GRB2-associated regulator of MAPK1 subtype 1(GAREM1), growth factor receptor-bound protein 2(GRB2), and SOS Ras/Rac guanine nucleotide exchange factor 1 (SOS1), activating the RAS/RAF/MAPK signaling cascade to promote oncogenesis. ChIP-qPCR revealed that E

conclusionOur research uncovers a novel KCNQ3-driven oncogenic axis in PTC, establishing KCNQ3 as a promising therapeutic target. Our findings also establish E

Indexed as

ESR1KCNQ3Papillary thyroid cancerRAS/RAF/MAPK signaling pathwayXE991

Identifiers

PMID41250218
PMCPMC12625505

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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.