Evidence map›Paper›PMID 40686241›Full record

ArticleFuture science OA2025

PAR2 regulates proliferation, migration of lung cancer and chemotherapy sensitivity by involving PTEN pathway.

Mei Zhai, Hua Xue, Feng Li

Abstract read
In one paragraph

Article in Future science OA, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
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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

3 authors.

Mei ZhaiThe First People's Hospital of Xianyang, Xianyang, Shaanxi, China.
Hua XueThe First People's Hospital of Xianyang, Xianyang, Shaanxi, China.
Feng LiThe First People's Hospital of Xianyang, Xianyang, Shaanxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProtease-activated receptor 2 (PAR2) is associated with tumor growth and metastasis. Here we examined the functions of PAR2 on growth, migration, invasion and chemosensitivity using both lung cancer cells and human lung cancer tissue.

methodsThe effect of PAR2 on growth of lung cancer cells was examined by MTT assay. The function of PAR2 on migration and invasion of lung cancer cells was evaluated by transwell migration and matrigel invasion assays. The role of PAR2 on paclitaxel-induced apoptosis was evaluated by Caspase-Glo3/7 assay. PAR2 levels in human lung cancer tissue were measured by qRT-PCR assay.

resultsOverexpression of PAR2 increased the proliferation, promoted migration and invasion in lung cancer cells. Up-regulation of PAR2 decreased the paclitaxel treatment sensitivity in lung cancer cells. PAR2 decreased paclitaxel-induced apoptosis by regulation of BAX and Bcl-2 expression. Aberrant expression of PTEN and p-AKT in lung cancer cells was impacted by PAR2. Serum PAR2 levels were increased in lung cancer patients. PAR2 expression was higher in human lung cancer tissue than normal lung tissues and associated with cancer stage.

conclusionsPAR2 displayed essential roles in lung carcinogenesis and might act as a potential biomarker to predict chemotherapy response and prognosis in lung cancer.

Indexed as

apoptosischemotherapylung cancerPAR2PTEN

Identifiers

PMID40686241
PMCPMC12296048

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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.