ArticleFrontiers in oncology2026
Acidic microenvironment-induced LAMC2 expression promotes proliferation, migration, and pathway regulation in non-small cell lung cancer cells.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aims to investigate the regulatory mechanism by which the acidic microenvironment modulates LAMC2 expression in non-small cell lung cancer (NSCLC) and to elucidate its roles in tumor cell proliferation, migration, invasion, and associated signaling pathways, thereby providing a theoretical foundation for targeted lung cancer therapies. Methods: A cohort of 104 pathologically confirmed NSCLC patients treated at a designated hospital from January 2018 to December 2021 was enrolled. RNA-seq data from the TCGA database were analyzed to evaluate LAMC2 expression differences and prognostic implications using the GEPIA2 tool. Results: The LAMC2 mRNA levels were elevated across multiple tumor types and correlated with unfavorable prognoses in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). The acidic microenvironment significantly upregulated LAMC2 expression through HIF-1α-mediated transcriptional activation. LAMC2, in turn, promoted NSCLC cell proliferation, migration, and invasion by activating the PI3K/Akt signaling pathway and inducing epithelial-mesenchymal transition (EMT). Clinically, a high LAMC2 expression was associated with poor tumor differentiation, advanced TNM staging, and reduced 3-year survival rates. Moreover, LAMC2 positively correlated with immune checkpoint molecules (e.g., PD-L1, CTLA-4), implying its involvement in immune evasion. Conclusion: The acidic microenvironment upregulates LAMC2 via HIF-1α-mediated transcriptional regulation and lactate accumulation, thereby driving malignant progression in NSCLC. Elevated LAMC2 levels are linked to enhanced proliferation, migration, invasion, and dismal patient outcomes, underscoring its potential as a therapeutic target for precision oncology.
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.