MID1 (Midline 1)

MID1IP1 promotes CRC cell survival by stabilizing c-Myc and preventing ferroptosis, while also influencing migration. These findings suggest that MID1IP1 may serve as a novel biomarker and therapeutic target in CRC.

The research results show that through the comprehensive analysis of biomedical images and gene expression profile data, we found the sharing function between central neurons and breast cancer. The central neuronal cell marker genes EMID1 and GREB1L may be used as key biomarkers to regulate the pathogenesis of breast cancer and affect the occurrence and development of breast cancer.

Moreover, the expression levels of UBE2C in CTCs were higher than other cells and tissues, indicated that UBE2C may affect the BCR event of PCa patients through CTCs. Our findings demonstrated that CRGs were significantly associated with BCR and immunotherapy efficacy in PCa and CRGs may influence the BCR event through CTCs.

The enrichment analysis results suggested that the relevant signaling pathways were potentially involved in the development of RILI. Further validation of those genes and signaling pathways is needed to confirm these findings.

Our study identified MID1IP1 as a regulator in promoting FRA1 mediated-MMP9 signaling and demonstrated its role in HCC metastasis. Targeting MID1IP1-mediated FRA1 pathway may serve as a potential therapeutic strategy against HCC progression.

In addition, TA3 enhanced the apoptotic effects of doxorubicin and 5-FU in colon cancer cells. Altogether, our results reveal a mechanism by which TA3 induces apoptosis through inhibiting c-Myc expression via CNOT2 or MID1IP1 in HCT116, which may help in the development of new therapies for colon cancer based on TA3 in the future.

In all, this study helps to understand the immune microenvironment of LUAD and improve the survival of patients with LUAD. Thus, EMID1 may be a novel immune-related prognostic marker of LUAD.