Evidence map›Paper›PMID 34090445›Full record

ArticleCancer cell international2021

FOXH1 promotes lung cancer progression by activating the Wnt/β-catenin signaling pathway.

Jun Zhang, Xian Zhang, Shasha Yang, Yanqiu Bao, Dongyuan Xu, Lan Liu

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

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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 2 institutions in 1 country.

Jun Zhang *Department of Morphological Experiment Center, Medical College of Yanbian University, Yanji, Jilin, 133000, China.
Xian Zhang *Department of General Surgery, Affiliated Hospital of Yanbian University, Yanji, Jilin, 133000, China.
Shasha YangDepartment of Morphological Experiment Center, Medical College of Yanbian University, Yanji, Jilin, 133000, China.
Yanqiu BaoDepartment of Pathology, Affiliated Hospital of Yanbian University, Yanji, Jilin, 133000, China.
Dongyuan XuDepartment of Morphological Experiment Center, Medical College of Yanbian University, Yanji, Jilin, 133000, China. dyxu@ybu.edu.cn.ORCID http://orcid.org/0000-0002-3055-6320
Lan LiuDepartment of Pathology, Affiliated Hospital of Yanbian University, Yanji, Jilin, 133000, China. lliu@ybu.edu.c.
Yanbian University · CNYanbian University Hospital · CN

Funding

National Natural Science Foundation of China 31760330National Natural Science Foundation of China 31860321National Natural Science Foundation of China 81560400
6 · The paper itself

Abstract

backgroundThe expression of forkhead box protein H1 (FOXH1) is frequently upregulated in various cancers. However, the molecular mechanisms underlying the association between FOXH1 expression and lung cancer progression still remain poorly understood. Thus, the main objective of this study is to explore the role of FOXH1 in lung cancer.

methodsThe Cancer Genome Atlas dataset was used to investigate FOXH1 expression in lung cancer tissues, and the Kaplan-Meier plotter dataset was used to determine the role of FOXH1 in patient prognosis. A549 and PC9 cells were transfected with short hairpin RNA targeting FOXH1 mRNA. The Cell Counting Kit-8, colony formation, soft agar, wound healing, transwell invasion and flow cytometry assays were performed to evaluate proliferation, migration and invasion of lung cancer cells. Tumorigenicity was examined in a BALB/c nude mice model. Western blot analysis was performed to assess the molecular mechanisms, and β-catenin activity was measured by a luciferase reporter system assay.

resultsHigher expression level of FOXH1 was observed in tumor tissue than in normal tissue, and this was associated with poor overall survival. Knockdown of FOXH1 significantly inhibited lung cancer cell proliferation, migration, invasion, and cycle. In addition, the mouse xenograft model showed that knockdown of FOXH1 suppressed tumor growth in vivo. Further experiments revealed that FOXH1 depletion inhibited the epithelial-mesenchymal transition of lung cancer cells by downregulating the expression of mesenchymal markers (Snail, Slug, matrix metalloproteinase-2, N-cadherin, and Vimentin) and upregulating the expression of an epithelial marker (E-cadherin). Moreover, knockdown of FOXH1 significantly downregulated the activity of β-catenin and its downstream targets, p-GSK-3β and cyclin D1.

conclusionFOXH1 exerts oncogenic functions in lung cancer through regulation of the Wnt/β-catenin signaling pathway. FOXH1 might be a potential therapeutic target for patients with certain types of lung cancer.

Indexed as

EMTFOXH1Lung cancerProliferationβ-catenin

Identifiers

PMID34090445
PMCPMC8180118
OpenAlexW3167447661

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.