ArticleFrontiers in cell and developmental biology2026
ITGA5 is overexpressed and promotes tumor progression through SNAI2 in OSCC.
Article in Frontiers in cell and developmental biology, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Integrin subunit α5 (ITGA5) has been recognized as a potential diagnostic biomarker across multiple cancer types. ITGA5 is upregulated in head and neck squamous cell carcinoma (HNSCC). Oral squamous cell carcinoma (OSCC), with poor prognosis and high mortality, accounts for two-thirds of HNSCC cases. However, the biological functions and underlying mechanisms of ITGA5 in OSCC progression remain unclear. In the present study, we analyzed the expression, prognostic significance, function, and co-expression genes of ITGA5 in HNSCC using a series of public biological information databases, detected the role of ITGA5 in OSCC progression, and discussed the underlying mechanisms. The results indicate that both the mRNA and protein level of ITGA5 were upregulated and related to the prognosis of HNSCC. Knockdown of ITGA5 inhibited cell proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT). However, overexpression of snail family transcriptional repressor 2 (SNAI2) reversed the function of ITGA5 in regulating OSCC cell proliferation, invasion, migration, and EMT. In conclusion, our study suggests that ITGA5 is upregulated in HNSCC and associated with poor prognosis; functional studies indicate ITGA5 promotes OSCC proliferation and metastasis via SNAI2, indicating that ITGA5 may be a potential therapeutic target for OSCC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.