Evidence map›Paper›PMID 35116524›Full record

ArticleTranslational cancer research2021

Procyanidins mediates antineoplastic effects against non-small cell lung cancer via the JAK2/STAT3 pathway.

Yue Wu, Chi Liu, Yuxu Niu, Jiamin Xia, Liwen Fan, Yun Wu, Wen Gao

Open access · diamondAbstract read
In one paragraph

Article in Translational cancer research, 2021. 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
1.0field-weighted citation impact, top 21% 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, 16 citations in OpenAlex.

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  4. Procyanidin B2-induced LKB1-AMPK activation mitigates vascular smooth muscle cell proliferation through inhibition of mTOR signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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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

7 authors at 3 institutions in 1 country.

Yue Wu *Shanghai Key Laboratory of Clinical Geriatric Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Chi Liu *Shanghai Key Laboratory of Clinical Geriatric Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Yuxu Niu *Shanghai Key Laboratory of Clinical Geriatric Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Jiamin XiaMinistry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Liwen FanShanghai Key Laboratory of Clinical Geriatric Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Yun WuShanghai Key Laboratory of Clinical Geriatric Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Wen GaoShanghai Key Laboratory of Clinical Geriatric Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Huadong Hospital · CNFudan University · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is a malignant tumor with one of the highest rates of cancer-related morbidity and mortality worldwide. Non-small cell lung cancer (NSCLC) account for 85% of all lung cancers and have a poor prognosis. Proanthocyanidins (PCs) are polyphenolic compounds that are found widely in natural plants. The present study aimed to determine the effects of PC on lung cancer and identify its possible mechanism.

methodsA cell growth assay was used to detect the cell growth ability of A549 cancer cells, and a clonal formation assay was used to detect the cloning ability of A549 cancer cells. Flow cytometry was used to detect the effect of PCs on apoptosis and the cell cycle. The wound healing test, Transwell migration, and invasion test were used to detect the migration and invasion of human NSCLC A549 cells. Western blotting was utilized to detect the expression levels of N-cadherin, E-cadherin, vimentin, Janus kinase 2 (JAK2), p-signal transducer and activator of transcription 3 (p-STAT3), STAT3, matrix metalloproteinase 2 (MMP-2), MMP-9, and the apoptosis-related proteins, B-cell lymphoma-2 (Bcl-2) and BCL2-associated X (Bax). Cell immunofluorescence was used to detect the expression levels of the p-STAT3 primary antibody.

resultsPCs reduced the proliferation and cloning ability of A549 cells and significantly inhibited the migration and invasion of A549 cells in a dose-dependent manner. At the same time, PCs induced apoptosis in A549 cells and G2/M cell cycle arrest. PCs increased the pro-apoptotic protein expression, Bax, and down-regulated the anti-apoptotic protein expression, Bcl-2. PCs also inhibited the epithelial-mesothermal transition (EMT) process of A549 cells. We also found that the JAK2/STAT3 signaling pathway inhibitor, AG490, cooperated with PCs to inhibit A549 cell invasion and migration. Our results demonstrated that PCs could mediate the antitumor effect of NSCLC via the JAK2/STAT3 pathway.

conclusionsPCs can inhibit NSCLC A549 cell proliferation, invasion, metastasis, clone formation, EMT, and induced apoptosis and G2/M cell cycle arrest. They work by inhibiting the JAK2/STAT3 signaling pathway. As a novel antitumor drug, PCs have broad application prospects for the treatment of NSCLC.

Indexed as

epithelial-mesothermal transition (EMT)Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3)non-small cell lung cancer (NSCLC)Proanthocyanidins

Identifiers

PMID35116524
PMCPMC8797329
OpenAlexW3160655147

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.