CEMIP (Cell Migration Inducing Hyaluronidase 1)

Furthermore, CHX chase assays showed that CEMIP and c-MYC mutually stabilized the expression of both proteins. The elevated CEMIP/c-MYC axis accelerates EMT to enhance cell migration, thereby contributing to the acquisition of gefitinib resistance in LUAD.

These data indicate that CEMIP blocks remyelination by generating bioactive HA fragments that inhibit OPC maturation. CEMIP is therefore a potential target for therapies aimed at promoting remyelination.

This review examines the role of exosomal proteins in key mechanisms that directly contribute to cancer dissemination to distant organs. This review also highlights the emerging relevance of exosomal proteins as diagnostic indicators of metastasis and as potential therapeutic targets, positioning them as future dual-purpose tools to improve both detection and intervention strategies in metastatic disease.

However, the molecular mechanisms by which KIAA1199 regulates chemoresistance, prognosis, and cancer stem cell development remain incompletely understood. Therefore, this review aims to summarize the clinical relevance of KIAA1199 as a novel regulator involved in chemoresistance, cancer prognosis, and cancer stem cell biology.

These results are better than that of serum CEA, which was 75% sensitive and 60% specific, with AUC of 0.52 and that of serum CA 19 - 9, which was 60% sensitive and 58% specific, with AUC of 0.56. Serum CEMIP may serve as non-invasive biomarkers for diagnosis of pancreatic cancer patients in comparison to other conventional biomarkers.

Our findings demonstrate that the ELK4-METTL3-CEMIP axis enhances the development of CRC. Targeting the axis may lead to the development of novel strategies against CRC.

HYBID expression is upregulated by proinflammatory factors such as histamine and interleukin-6 and downregulated by transforming growth factor-β. HYBID is involved in physiological HA turnover in human skin and joint tissues and plays an important role in their pathological destruction by accelerating HA degradation.

CIP2A targets CEMIP to activate NF-κB signaling pathway, which in turn aggravates cartilage destruction and inflammation and ultimately accelerates OA development. Our results suggest the potential role of the CIP2A/CEMIP axis as a therapeutic target for OA.

These findings emphasize the potential of ANGPT2 and CEMIP as biomarkers for LC progression and prognosis. To our knowledge, no previous study has evaluated the presence and quantification of ANGPT2 and CEMIP in EV cargo from lung cancer patients. To further validate their role in cancer progression, functional studies should explore the mechanistic effects of EV-associated ANGPT2 and CEMIP on angiogenesis, immune modulation, cell migration, extracellular matrix remodeling, and tumor progression in lung cancer models.

MARCH8 promoted CRC cell ferroptosis via inhibiting PI3K/AKT pathway by enhancing the ubiquitination and degradation of CEMIP.

Besides, these genes can be incorporated into clinical prognostic models, offering panels of genes to choose appropriate personalized methods of treatment. Together, these genes represent novel markers and possible therapeutic targets for CRC.

Bexarotene potentially exerts its anti-tumor effect by reducing HA levels through decreased expression of HAS. These findings provide new insights into the process of CTCL development and additional insights regarding bexarotene treatment.