Evidence map›Paper›PMID 36385523›Full record

ArticleCancer gene therapy2023

KCNF1 promotes lung cancer by modulating ITGB4 expression.

Ching-Yi Chen, Pei-Ying Wu, Michelle Van Scoyk, Stephanie A Simko, Chu-Fang Chou, Robert A Winn

Open access · hybridFull text read
In one paragraph

Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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  6. Review
  7. Article
  8. Translational lung cancer research · 2024
    Article
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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 1 institution in 1 country.

Ching-Yi ChenMassey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.ORCID 0000-0002-1978-6424
Pei-Ying WuMassey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.
Michelle Van ScoykMassey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.ORCID 0000-0001-6631-8300
Stephanie A SimkoMassey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.
Chu-Fang ChouMassey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.
Robert A WinnMassey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA. robert.winn@vcuhealth.org.ORCID 0000-0001-5948-9291
Virginia Commonwealth University · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Kim Felder Rhoads · 1985 to 2026
$51.0M
Role of the noncanonical WNT pathway in non-small cell lung cancerR01CA138528 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI WINN, ROBERT A. · 2010 to 2014
$1.4M
Targeted investigation of tissue specific oxidative stress in the etiology of ALSI01BX000517 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI VAN REMMEN, HOLLY · 2011 to 2013
–
BLRD VA I01 BX000517NCI NIH HHS P30 CA016059NCI NIH HHS R01 CA138528
6 · The paper itself

Abstract

Lung cancer continues to be the leading cause of cancer death in the United States. Despite recent advances, the five-year survival rate for lung cancer compared to other cancers still remains fairly low. The discovery of molecular targets for lung cancer is key to the development of new approaches and therapies. Electrically silent voltage-gated potassium channel (KvS) subfamilies, which are unable to form functional homotetramers, are implicated in cell-cycle progression, cell proliferation and tumorigenesis. Here, we analyzed the expression of KvS subfamilies in human lung tumors and identified that potassium voltage-gated channel subfamily F member 1 (KCNF1) was up-regulated in non-small cell lung cancer (NSCLC). Silencing of KCNF1 in NSCLC cell lines reduced cell proliferation and tumor progression in mouse xenografts, re-established the integrity of the basement membrane, and enhanced cisplatin sensitivity. KCNF1 was predominately localized in the nucleoplasm and likely mediated its functions in an ion-independent manner. We identified integrin β4 subunit (ITGB4) as a downstream target for KCNF1. Our findings suggest that KCNF1 promotes lung cancer by enhancing ITGB4 signaling and implicate KCNF1 as a novel therapeutic target for lung cancer.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansIntegrin beta4MicePotassium Channels, Voltage-GatedSignal TransductionIntegrin beta4ITGB4 protein, humanKCNF1 protein, humanPotassium Channels, Voltage-Gated

Identifiers

PMID36385523
PMCPMC10014577
OpenAlexW4309409152

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read46
Read underepoch 390

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.