RASD1 (Ras Related Dexamethasone Induced 1)

RASD1 is frequently silenced in MM through promoter hypermethylation. This epigenetic inactivation is associated with adverse clinical features and enhanced cell survival, supporting a tumor suppressor role for RASD1 in MM pathogenesis.

Furthermore, the expression of genes exhibiting similar expression patterns as RASD1 suggest that RASD1 may play a role in interleukin-4-mediated apoptosis and could regulate the transcription of the phosphatase and tensin homolog (PTEN) gene. Overall, these findings suggest that RASD1 may modulate immune signaling and tumor suppressive pathways.

The "Zhibian" (BL54)-to-"Shuidao" (ST28) needling technique may ameliorate the decline of ovarian response in mice with POR, promote normal follicle development and ovulation, thereby improve embryo quality and reduce the risk of developmental defects and deformity in the organs such as the embryonic heart. The underlying mechanism may be related to the regulation of the expression pattern of embryonic key genes through the Wnt signaling pathway.

In conclusion, SIX1-1 promoted cervical cancer cell proliferation by modulating RASD1 expression. This suggests that targeting the SIX1-1/RASD1 axis could be a potential antitumor strategy for cervical cancer.

KIAA1429 plays a pro‑oncogenic role in GC by downregulating RASD1 expression through destabilizing RASD1 mRNA in an m6A-YTHDF2-dependent manner. KIAA1429 may serve as a prognostic biomarker and therapeutic target for GC.

It can be concluded that Rasd1 exerts a modulated role in oligodendrocytes ferroptosis in WMI following SAH.