ArticleCancer immunology, immunotherapy : CII2026
IL-6 as a driver of bone invasion in IFIT2-depleted oral squamous cell carcinoma.
Article in Cancer immunology, immunotherapy : CII, 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
Abstract
Oral squamous cell carcinoma (OSCC), the most prevalent oral cancer, often exhibits local bone invasion. Interferon-induced protein with tetratricopeptide repeats 2 (IFIT2) has been identified as a tumor suppressor in OSCC, though its role in bone invasion remains unclear. This study aimed to investigate the involvement of IL-6 as a driver of bone invasion in OSCC with depleted IFIT2 expression and to evaluate the clinical relevance of IFIT2 and IL-6. IFIT2 knockdown significantly increased IL-6 mRNA and secretion levels in OSCC cells, indicating IFIT2's potential regulatory role in inflammation within the tumor microenvironment. Elevated IL-6 levels in IFIT2-depleted OSCC cells markedly enhanced osteoclast differentiation and bone resorption. Neutralizing IL-6 reversed these effects, confirming IL-6 as a key mediator of bone invasion in OSCC cells. These results indicate that IL-6 as driver of bone invasion in IFIT2-depleted OSCC cells. Clinically, serum IL-6 concentrations were significantly higher in patients with advanced-stage tumors (T4) compared to early stages (T1-3; p = 0.027), supporting IL-6's role as a progression marker. Stage IV OSCC patients exhibited higher IL-6 levels compared to stages I-III, further substantiating IL-6's prognostic significance in advanced OSCC (p = 0.043). Serum IL-6 positively correlated with pro-tumorigenic cytokines, including VEGF-α and G-CSF. Notably, a high IL-6/IFIT2 ratio was associated with reduced median survival among OSCC patients. These findings indicate that IFIT2 depletion enhances OSCC-induced bone invasion predominantly through IL-6-mediated osteoclast activation, establishing the IL-6/IFIT2 axis as a critical regulator of OSCC progression and metastasis.
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.