Evidence map›Paper›PMID 35117647›Full record

ArticleTranslational cancer research2020

Hypoxia induces tumor cell growth and angiogenesis in non-small cell lung carcinoma via the Akt-PDK1-HIF1α-YKL-40 pathway.

Yushan Miao, Wei Wang, Yaping Dong, Jiaxun Hu, Kunchen Wei, Shuo Yang, Xueli Lai, Hao Tang

Open access · diamondAbstract read
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Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

11 citing papers in PubMed, 13 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

8 authors at 3 institutions in 1 country.

Yushan Miao *Department of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Wei Wang *Department of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Yaping Dong *The Graduate School of Fujian Medical University, Fuzhou 350122, China.
Jiaxun HuDepartment of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Kunchen WeiDepartment of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Shuo YangDepartment of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Xueli LaiDepartment of Nephrology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai 200433, China.
Hao TangDepartment of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Second Military Medical University · CNChanghai Hospital · CNFujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAs one of the most common forms of cancer, non-small cell lung carcinoma (NSCLC), is characterized by oxygen deprivation (hypoxia). The transcription factor hypoxia-inducible factor (HIF)-1α is a major mediator which responds hypoxia and regulates many contributing factors. The various modes of hypoxia regulation are frequently the focus of research studies. With reference to previous published research, we hypothesized that hypoxia promotes the growth and angiogenesis of NSCLC via the Akt-PDK1-HIF1α-YKL-40 pathway, and verified it.

methodsWe mainly investigated changes in related factor expression between differently treated CL1-5 cells. We carried out overexpression and underexpression transfection, Western blot, rt-PCR and ELISA, and observed cellular biological behaviors by CCK-8 migration and invasion assay, and tube formation assay.

resultsA hypoxic environment significantly increased the phosphorylation of Akt and PDK1 in mitochondria. The hypoxia-induced accumulation of p-Akt in mitochondria activated PDK1 phosphorylation, promoted the expression of HIF1α, and the expression of YKL-40. The overexpression of YKL-40 promoted the proliferation, migration, invasion and tubule formation of CL1-5 cells.

conclusionsA hypoxic tumor microenvironment can promote the expansion and angiogenesis of NSCLC cells through the Akt-PDK1-HIF1α-YKL-40 pathway. This may provide a new mechanism and potential interventional target for anti-vascular lung cancer therapy.

Indexed as

AktHypoxiahypoxia-inducible factor-1α (HIF-1α)non-small cell lung carcinoma (NSCLC)YKL-40

Identifiers

PMID35117647
PMCPMC8799056
OpenAlexW3071328941

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.