Evidence map›Paper›PMID 33943003›Full record

ArticleJournal of cellular and molecular medicine2021

HIF-1α is necessary for activation and tumour-promotion effect of cancer-associated fibroblasts in lung cancer.

Yana Zhang, Yangyang Bian, Yuan Wang, Yuanyuan Wang, Xixi Duan, Yuning Han, Lijing Zhang, Fei Wang, Zhuoyu Gu, Zhihai Qin

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  3. The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026
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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

10 authors at 3 institutions in 1 country.

Yana ZhangMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yangyang BianMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yuan WangMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yuanyuan WangMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xixi DuanMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yuning HanGeneral Hospital of Ningxia Medical University, Ningxia, China.
Lijing ZhangMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Fei WangMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Zhuoyu GuMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Zhihai QinMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0000-0001-9793-7964
Henan Cancer Hospital · CNChinese Academy of Sciences · CNNingxia Medical University · CN

Funding

National Natural Science Foundation of China 81630068National Natural Science Foundation of China 82073231
6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) activation is crucial for the establishment of a tumour promoting microenvironment, but our understanding of CAFs activation is still limited. In this study, we found that hypoxia-inducible factor-1α (HIF-1α) was highly expressed in CAFs of human lung cancer tissues and mouse spontaneous lung tumour. Accordingly, enhancing the expression of HIF-1α in fibroblasts via hypoxia induced the conversion of normal fibroblasts into CAFs. HIF-1α-specific inhibitor or HIF-1α knockout (KO) significantly attenuated CAFs activation, which was manifested by the decreased expression of COL1A2 and α-SMA. In vivo, during tumour formation, the expression of Ki-67 and proliferating cell nuclear antigen (PCNA) in the tumour tissue with HIF-1α KO fibroblasts was significantly lower than that of normal fibroblasts. Moreover, HIF-1α in fibroblasts could activate the NF-κB signalling pathway and enhance a subsequent secretion of CCL5, thus promoting the tumour growth. In conclusion, our results suggest that HIF-1α is essential for the activation and tumour-promotion function of CAFs in lung cancer (LC). And targeting HIF-1α expression on CAFs may be a promising strategy for LC therapy.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorCancer-Associated FibroblastsCarcinoma, Lewis LungCell ProliferationFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitLung NeoplasmsMiceMice, Inbred C57BLSignal TransductionTumor Cells, CulturedTumor MicroenvironmentBiomarkers, TumorHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitCAFsCCL5fibroblastsHIF-1αlung cancer

Identifiers

PMID33943003
PMCPMC8184678
OpenAlexW3157375481

What OpenQuestion holds

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LicenceCC BY
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.