MT2A (Metallothionein 2A)

Silencing circEIF6 suppressed glycolysis, angiogenesis, and proliferation (P<0.05) by sponging miR-296-3p to downregulate MT2A. We conclude that circEIF6 promotes aerobic glycolysis and angiogenesis in TNBC via the miR-296-3p to target MT2A.

Mechanistically, we reveal that copper ion is also essential for hypoxia-induced mitochondrial translocation of Pyruvate kinase M2 (PKM2), and facilitates the interaction of MT2A with the tetrameric form of PKM2 to maintain its activity, thereby promoting glycolysis and oxidative phosphorylation. Thus, our findings reveal the MT2A-copper-PKM2 axis as a potential therapeutic target to treat breast cancer.

Conversely, OSCC cells from smokers exhibit resistance to Cd toxicity, likely due to the overexpression of metallothionein 2A (MT2A), a heavy metal detoxification protein. Collectively, this study provides the evidence that ferritinophagy may act as a critical upstream driver of Cd-induced ferroptosis in OSCC cells derived from never-smokers, paving the way for potential ferroptosis-targeted therapeutic strategies in Cd-associated malignancies.

The direct interactions of either MT2P1/miR-15b-5p or miR-15b-5p/MT2A were, respectively, ascertained, enlightening the ceRNA effect of them. The pseudogene-derived MT2P1-RNA is a suppressor of HCC by exerting the ceRNA effect on preserving MT2A, and its transcription is regulated by the suppressive transcription factor E2F7.

MT2A facilitates the migration and invasion of SCLC cells by influencing the YAP1 signaling cascade. This investigation offers a fresh avenue for delving deeply into the potential mechanisms involved in the progression of SCLC.

53BP1 plays a crucial role in maintaining ROS homeostasis by regulating genes involved in oxidative stress response. These results suggest that targeting ROS regulation through 53BP1-related pathways may provide novel insights into therapeutic strategies for diseases associated with oxidative stress.

Knockdown of SLC7A5 inhibits malignant progression and attenuates oxaliplatin resistance in GC by suppressing glycolysis.

Super-resolution imaging of MDA-MB-231 cells shows that the downregulation of MT2A and DIAPH3 inhibits cell polarization and thereby migration, suggesting that MT2A may regulate motility via DIAPH3-dependent cytoskeletal remodeling. In summary, our strategy enables the de novo discovery of PROTACs and ligands for novel disease-related targets and lays the groundwork for expansion of the druggable proteome.

JPJDR regulates a range of cell types in the CRC microenvironment, including malignant CRC, immune cells and stromal cells. Downregulation of HMGB1 and MT2A might be the important mediators for JPJDR to modulate the CRC microenvironment.

The nuclear stain Hoechst 33342, assessed by fluorescence microscopy, provides a low variance, moderate throughput platform for cancer cell loss screens. Low metallothionein ovarian cancer cells exhibit a vulnerability to the RAF inhibitor encorafenib.

These findings indicated that intervention with 125I radiation particles may induce changes in gene expression, potentially influencing alterations in biological characteristics. In conclusion, these insights may shed light on the underlying mechanisms of 125I radiation particle therapy in HCC and offer novel targets for HCC treatment.

Targeting glutamine metabolism in combination with metformin is a promising new therapeutic strategy for AML.