MT1G (Metallothionein 1G)

Consequently, this cascade promoted RCC progression. In conclusion, our findings indicate that SAP30 inhibits the p53 pathway through MT1G suppression, suggesting that SAP30 and MT1G are potential prognostic markers and therapeutic targets for RCC.

METTL3-mediated m6A modification of MT1G inhibited PTC cell growth and metastasis via inactivating the Wnt/β-catenin pathway.

The AUC value of the nomogram for training and validation set was 0.802 (95% CI 0.750-0.855) and 0.718 (95% CI 0.624-0.811). Moreover, the nomogram has outstanding calibration and actual clinical patient benefits.ConclusionsWe identified a nomogram based on the 3-gene signature and clinical characteristics that effectively predicted LNM in PTC patients, which offers guidance for the preoperative assessment the appropriate scope of operation in PTC patients.

Overexpression of MT1G inhibits GPX4, thereby affecting SQSTM1 as a vector to promote ARNTL autophagy and EGLN2, promoting ARNTL clock autophagy through the GPX4/SQSTM1 axis. Our research findings elucidate that overexpression of MT1G promotes iron autophagy centered around ARNTL in GC cells via the GPX4/SQSTM1 axis, thereby inhibiting GC cell function and providing a new molecular mechanism and therapeutic target for the development of GC.

Our study unveils a novel mechanism of lipid droplet accumulation in ccRCC, where MT1G inhibits CPT1B expression through modulation of H3K14 trimethylation, consequently enhancing lipid droplet accumulation and promoting ccRCC progression. Graphical abstract figure Schematic diagram illustrating MT1G/H3K14me3/CPT1B-mediated lipid droplet accumulation promoted ccRCC progression via FAO inhibition.

This research identified MT1G as a potential biomarker for OS prognosis, highlighting its potential as a therapy target.

We also showed that the combination of artesunate and doxorubicin had a marked additive inhibitory effect on GCB and ABC DLBCL cells. In conclusion, artesunate induces ferroptotic death in GCB and ABC DLBCL cells by attenuating the GPX4/GSH antioxidant defence system and increasing intracellular iron levels, indicating its therapeutic potential for relapsed or refractory DLBCL.

Moreover, MT1G also counteracted the BA-induced changes in cell cycle-related proteins (CDK2 and CDK4) and p-Rb. In summary, we have revealed a new anti-tumor mechanism that BA altered the cell cycle progression of CRC cells by upregulating MT1G gene, thereby inhibiting the proliferation of CRC cells.

Our study elucidates the pivotal role played by MT1G in the pathogenesis of prostate cancer (PCA) and its profound implications for prognosis. Moreover, it raises the intriguing possibility that MT1G could pave the way for novel therapeutic approaches in PCA treatment. This potential arises from its ability to orchestrate immune infiltration within the tumor microenvironment, consequently enhancing sensitivity to immune checkpoint inhibitor (ICI) therapy. Therefore, our findings hold substantial promise for advancing our comprehension of PCA and exploring innovative therapeutic strategies.