CMTM4 (CKLF Like MARVEL Transmembrane Domain Containing 4)

Additionally, CMTM4 overexpression was associated with a reduction in MDSC infiltration within cervical tumor tissues. CMTM4 emerges as a critical regulator in cervical cancer, influencing both tumor cell behavior and the immune microenvironment.

This comprehensive transcriptomic characterization of T-cell exclusion in PM reveals that targeting cilium-based Hedgehog signaling, in addition to multiple other actionable drug targets, could enhance the efficacy of ICB treatment in PM.

CMTM4 is often downregulated in colorectal cancer and exhibits tumor-suppressive properties. These findings indicate that CMTM4 may serve as a potential therapeutic target for colorectal cancer.

The combination of CMTM4 inhibition and anti-PD-1 treatment shows promising antitumor efficacy against CC. These findings offer novel insights into the tumor microenvironment and have the potential to inform the development of innovative immunotherapy approaches for CC.

Notably, eltrombopag is identified as a CMTM4 inhibitor that attenuates OC progression in vivo and modulates the tumor immune microenvironment, synergizing with PD-1 blockade immunotherapy to enhance therapeutic efficacy. The exosomal CMTM4-ICAM1-CD206 axis exacerbates disease risk in patients with OC. Collectively, the study highlights the critical role of tumor-derived exosomal CMTM4 in immune suppression, emphasizing its potential as both a prognostic biomarker and a therapeutic target in OC immunotherapy.

Specifically, it suppressed the expression of IL-17 receptor RC (IL-17RC) and its downstream signaling molecules, resulting in the inhibition of nuclear factor-κ B (NF-κB) activation and a decrease in NADPH oxidase-1 (NOX1) levels. These results suggest that Cmtm4 deletion suppresses H. pylori-induced gastric carcinogenesis and precancerous lesion formation, potentially through the regulation of IL-17RC/NF-κB/NOX1 signaling, which may represent a new target for the early prevention of GC.

There were differential expressions of CMTMs between ESCA and normal tissues. Furthermore, the expression of CMTMs was positively correlated with M2 macrophages, indicating a possibility that CMTMs may become a new immunotherapy target for ESCA.

All five genes were significantly downregulated in ccRCC tumors and mouse xenograft tumors. The results from this research demonstrate the oncogenic ability of miR-2355-5p and shed light on the possible mechanism by which this miRNA controls angiogenesis and tumor growth in VHL-deficient ccRCC.

Knockout of CMTM4 enhances immune checkpoint blockade or chemotherapy to further reduce lung tumor growth. These data suggest that CMTM4 represents a novel target for the inhibition of tumor inflammation, and improvement of the immune response and tumor drug sensitivity.

CXCL8 expression on invasion margin regions in post-operative tissues was also an inferior predictor of DFS in patients with LARC. In conclusion, CMTM4 may predict the nCRT response and outcomes in patients with LARC.

Our results suggest that CMTM4 plays a tumor-suppressive role in GC and may affect the growth, migration, and invasion of GC cells through the STAT1 signaling pathway. CMTM4 might have potential value as a prognosis marker and potential therapeutic target for GC therapy.

Combined expression of TGM2 and CMTM4 can be used as an indicator to evaluate the risk of metastasis and prognosis of OSCC.