TMEM158 (Transmembrane Protein 158)

Our findings demonstrated that the TMEM158-TGF-β pathway plays a central role in mediating the heightened sensitivity of TP53-deficient OS to USP14 inhibition. Targeting this pathway may represent a promising therapeutic strategy for precision treatment of osteosarcoma.

It also highlights emerging connections between TMEM proteins and the tumor microenvironment, emphasizing their potential as promising therapeutic targets. The novel findings underscore the key role of the TMEM protein family in overcoming chemoresistance and lay a foundation for the development of targeted therapeutic strategies in cancer treatment.

Acrylamide may drive CRC progression through dysregulated signaling and immune modulation. Validation across cohorts and experimental models is needed to confirm key targets and inform precision prevention. These findings highlight acrylamide's public health relevance and support regulatory efforts to limit exposure from dietary and environmental sources.

TMEM158 reduced the actin skeleton stiffness of ICC cells through activating Ras protein mediated generation of LA, which finally results in enhanced metastasis of ICC. Our work provides a preclinical evidence of concept for TMEM158 as a novel candidate inhibiting the metastasis of ICC.

Single-cell transcriptomic analysis reveals prognosis-related stromal signatures that potentiate the stratification of eCCA into proliferative, inflammatory and fibrotic, and neuronal phenotypes, which has important implications on molecular classification and exploring therapeutic targets in eCCA.

The RF model exhibited an accuracy of 0.97, a kappa value of 0.92, and an area under the curve (AUC) of 0.99 in the external validation dataset. The results of this study have identified biomarkers through ML algorithms which help to identify patients with CRC prone to metastasis.

Mechanistically, we demonstrated that TMEM158 positively regulates ABCG2 expression, which consequently contributes to drug resistance. In summary, we identified cfRNA TMEM158 as a potential diagnostic biomarker for ovarian cancer and elucidated the critical involvement of TMEM158-ABCG2 signaling axis in the development of doxorubicin resistance.

TMEM158 is highly expressed in lung cancer, is associated with hypoxia, and promotes EMT and cell migration. These findings suggest TMEM158 as a potential target for lung cancer therapies.

In summary, CH25H promotes autophagy and affects the malignant progression of LSCC through the PI3K-AKT pathway.

The underlying mechanism involves TMEM158 and TWIST1 directly interacting, stimulating the PI3K/AKT signaling pathway in LUAD cells. This investigation emphasizes the molecular functions of TMEM158 in LUAD progression and proposes targeting it as a promising treatment approach for managing LUAD.

Lack of TMEM158 reduced GC tumor growth. Collectively, TMEM158 accelerated GC cell proliferation by modulating the PI3K/Akt signaling pathway, making it a prospective biomarker for survival in GC patients.

The study identified some hub genes that could be useful in predicting prognosis and management in GC.