MACC1 (MET Transcriptional Regulator MACC1)

Notably, we highlight the potential regulatory role of ANK2 in the progression of CRC. This research provides theoretical support and new directions for early screening, diagnostic biomarker identification, and targeted therapy strategies for CRC.

Additionally, multivariate analysis indicated that the positive expression of MACC1, AGR2, and KAI1, alongside tumor stage and LNM stage, could serve as independent prognostic indicators for OS in individuals diagnosed with cervical squamous cell carcinoma. MACC1, AGR2, and KAI1 may represent potential metastatic and prognostic biomarkers, as well as promising therapeutic targets for squamous cell carcinoma of the cervix.

MiR-597-3p functions as a tumor suppressor in ovarian cancer by directly targeting MACC1, thereby inhibiting proliferation, invasion, and survival. These findings highlight the miR-597-3p/MACC1 axis as a potential therapeutic target and suggest miR-597-3p as a promising biomarker for ovarian cancer.

Moreover, MACC1-AS1 contributes to therapeutic resistance, conferring reduced sensitivity to chemotherapeutic agents such as 5-fluorouracil (5-FU), oxaliplatin, gemcitabine, and cisplatin, as well as to combination regimens including 5-fluorouracil and oxaliplatin (FOLFOX). This review provides an overview of the current knowledge surrounding MACC1-AS1 and highlights its potential as both a biomarker and a therapeutic target for future translational research.

Our findings suggest that this four-gene panel holds significant promise as a robust prognostic tool for breast cancer survival. This research paves the way for further investigations into targeted therapies and personalized medicine approaches in the management of breast cancer.

In this overarching review, we explore the significance of MACC1-AS1 as a potential cancer treatment target and biomarker. This study can potentially play an important role in the advancement of the field and confirm its potential clinical applicability.

Our findings delineate an integrated metastatic axis: MACC1 orchestrates (1) transcriptional upregulation of YKT6 to amplify exosome production, and (2) selective packaging of c-Met into exosomes that prime recipient cells for invasion. This dual regulatory mechanism highlights potential therapeutic targets for intercepting metastasis-specific exosome signaling in colorectal cancer.

Experimentally, inhibition of H4K20me3 formation caused increased MACC1 mRNA expression in HCT116 cells. Conclusions, we reported a potential ROS-mediated epigenetic regulation of MACC1 expression in CRC through altered histone methylation, as our data suggested an initial epigenetic silencing of MACC1, which was later partially reactivated under oxidative stress.

Database analysis revealed that CYP2S1 was upregulated in colorectal cancer and positively associated with better prognosis. In conclusion, these findings suggest that CYP2S1 represents a promising biomarker and therapeutic target for improving the prognosis and treatment of colorectal cancer.

Moreover, the expression of GLUT4 was significantly decreased in the two cell lines treated by 4.5 g/L or 9.0 g/L glucose with MACC1 knockdown. Additionally, MACC1 knockdown could inhibit high glucose-induced membrane translocation of GLUT4.ConclusionsMACC1 knockdown can attenuate glucose metabolism by inhibiting the membrane translocation of GLUT4 in CRC cells.

This five-gene panel could serve as a novel molecular tool for HPV-associated cervical adenocarcinoma detection.

Based on comprehensive bioinformatic analysis, MACC1 was identified as the most promising MRG candidate in EC. Systematic experimental validation, including both in vitro and in vivo approaches, demonstrated that MACC1 down-regulation significantly suppressed EC progression, highlighting its potential as a therapeutic target.