MIA (MIA SH3 Domain Containing)

Overall, we report that Sitagliptin and Linagliptin have significant anticancer potential towards KRAS-mutated PDAC. Furthermore, we recommend repurposing of more drugs to examine their anti-cancer potential towards these aggressive cancers and to overcome clinical resistance in the near future.

In vivo studies confirm its superior tumor targeting, prolonged retention, and excellent biosafety. These findings establish NIR-CBT-NP as a powerful tool for possible early detection of the FAPα-expressing tumors.

Ethylene plays a significant role in enhancing MIA biosynthesis, and we have found that it greatly induces the accumulation of anhydrovinblastine...Our findings reveal an ethylene-activated regulatory model consisting of CrEIN3 and CrEIL1 that integrates JA-induced BIS2 to cooperatively regulate MIA production in C. roseus, shedding light on the mechanism of ethylene signal regulating MIA biosynthesis. This research provides a foundation for understanding plant hormone regulation of alkaloid metabolism, which will contribute to future efforts in developing high-yielding MIAs in plant or yeast-based platforms.

This proof-of-concept study evaluated the cytotoxic effects of ECT using bleomycin (BLM) or cisplatin (CDDP) in combination with sotorasib in KRAS G12C-mutated MIA PaCa-2 and KRAS G12D-mutated PANC-1 pancreatic cancer cell lines. Combining ECT with sotorasib resulted in an additive effect on KRAS G12C-mutated MIA PaCa-2 cells, though no synergy was observed, likely due to the high intrinsic sensitivity to electric pulses. These results support the potential of combining physical and molecular therapies in a subset of pancreatic cancer patients and lay the groundwork for further in vivo studies to optimize treatment parameters and explore clinical translatability.

We observed a synergistic relationship between camptothecin and sotorasib in KRAS-mutated cancer cells. Furthermore, we recommend examining more natural compounds with chemotherapeutic potential to help overcome clinical resistance of approved chemotherapeutic drugs in the near future.

Some clinical and ultrasonic characteristics of breast cancer were significantly correlated with immune-related genes, such as NR3C2, SAA2, and CXCL9. Further analysis of these genes provides new ideas for the diagnosis and treatment of breast cancer.

Overall, the findings show the differential expression and function of p97/VCP and SVIP in pancreas ductal adenocarcinoma cells. The potential of the pancreatic cancer cells to migrate and invade altered when the two cell lines were transfected with p97/VCPsi and SVIPsi.

MIA plays a crucial role in SCAPs' migration and differentiation, suggesting its potential application in pulp-dentin regeneration therapies. Further studies are required to fully elucidate the underlying mechanisms.

The PL-loaded DTPS efficiently uptake by MIA PaCa-2 cancer cells, causing up to 80 % cell growth inhibition, reduced cell spheroids volume and increased dead cells by 58.3 %. These results indicate that the newly developed DTPS can effectively serve as a pH-responsive drug delivery system for efficient treatment of cancer.

Moreover, Ce6-PDT increased apoptotic and necrotic markers while decreasing vascular endothelial growth factor (VEGF) expression in MIA PaCa-2 and BxPC-3 pancreatic cancer cell lines. The approach of the WGS-PAM system shows the potential to investigate PDT effects on the mechanism of angiographic dynamics with high-resolution wide-field imaging modalities.

These findings pinpoint four crucial genes in BC progression, offering targets for further research and therapy. Their connections to immune infiltration and chemotherapy sensitivity underscore complex interactions in the tumor microenvironment.

Interestingly, NINJ2 also regulates mutant p53 expression, and the loss of NINJ2 promotes cell growth and migration in mutant p53-expressing MIA-PaCa2 cells. Together, these data indicate that the mutual regulation between NINJ2 and p53 represents a negative feedback loop, and the NINJ2-p53 loop has opposing functions in wild-type p53-dependent growth suppression and mutant p53-dependent growth promotion.