ArticleInternational journal of medical sciences2026
Cyr61 Promotes Oral Squamous Cell Carcinoma Cell Motility via an Integrin αvβ3/αvβ5-PLC/PKC/c-Src-AP-1-ICAM-1 Signaling Axis.
Article in International journal of medical sciences, 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
Oral squamous cell carcinoma (OSCC) frequently metastasizes, leading to poor patient outcomes. Cysteine-rich angiogenic inducer 61 (Cyr61/CCN1) has been implicated in cancer progression; however, the downstream mechanism driving OSCC motility remains incompletely defined. Cyr61 expression was elevated in OSCC and associated with advanced clinicopathological features. In OSCC cell lines, recombinant Cyr61 enhanced wound closure and Transwell migration and increased intercellular adhesion molecule-1 (ICAM-1) expression at both the mRNA and protein levels. ICAM-1 silencing significantly attenuated Cyr61-induced cell motility, indicating that ICAM-1 is an important downstream effector. Mechanistically, Cyr61 signaling was initiated through integrin αvβ3 and αvβ5, as neutralizing antibodies and siRNAs targeting these integrins suppressed Cyr61-induced migration and ICAM-1 expression. Cyr61 also induced phosphorylation of PLC, PKC, and c-Src, and pharmacological or siRNA-mediated inhibition of these kinases attenuated ICAM-1 upregulation and cell migration. Moreover, Cyr61 enhanced AP-1 activity via c-Jun phosphorylation, increased c-Jun occupancy at the ICAM-1 promoter, and inhibition of AP-1 signaling diminished Cyr61-driven ICAM-1 expression and motility. Together, these data define an integrin αvβ3/αvβ5-PLC-PKC-c-Src-AP-1 axis that transcriptionally upregulates ICAM-1, promoting OSCC migration and providing a mechanistic basis for targeting Cyr61-driven migratory programs in 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.