ArticleFrontiers in oncology2025
AMPs inhibit the proliferation, migration, and invasion of lung cancer via the CHRM3/PI3K/AKT and CHRM3/MAPK pathways.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Screening, validation, and mechanism study of antitumor components fromFrontiers in oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: Our previous studies indicated that the overexpression of M3 muscarinic receptor (M3R/CHRM3) is related to a poor prognosis in patients with lung cancer and that Materials and methods: Lung cancer cell lines (A549, NCI-H1299, and NCI-H520) with stable overexpression or knockdown of CHRM3 were established by infection with recombinant lentivirus and selected under puromycin for one month. Stable cells were treated with or without 100 μg/mL AMPs for 24 h or 48 h. The changes in CHRM3 expression, cell proliferation, migration, and invasion were determined. The expression levels of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) and mitogen-activated protein kinase (MAPK) pathway-related proteins were detected. The antitumor activity of AMPs was further assessed in a xenograft mouse model bearing A549 cells with stable CHRM3 knockdown. Results: CHRM3 was highly expressed in NCI-H520 cells and moderately expressed in A549 and NCI-H1299 cells. CHRM3 overexpression significantly increased while CHRM3 knockdown significantly decreased the cell proliferation, migration, and invasion. AMP treatment downregulated the expression of CHRM3 and decreased the cell proliferation, migration, and invasion. Moreover, CHRM3 overexpression significantly activated the PI3K/AKT and MAPK signaling pathways, whereas AMP treatment decreased CHRM3-induced PI3K/AKT and MAPK activation. In xenograft mice bearing A549 tumors, CHRM3 knockdown showed little inhibition on tumor growth, but AMP treatment inhibited the tumor growth. Conclusion: AMP treatment inhibits the proliferation, migration, and invasion of lung cancer via the CHRM3/PI3K/AKT and CHRM3/MAPK pathways, thus exerting antitumor activity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.