MARK2 (Microtubule Affinity Regulating Kinase 2)

Clinically approved drugs such as Dasatinib (targeting CSK) and Crizotinib (targeting MET) emerged as promising candidates due to favorable pharmacokinetics and known bioactivity. Host-directed therapeutics could offer alternative strategies to conventional antibiotic therapy, addressing challenges such as resistance and infection recurrence, providing a foundation for future experimental validation and development of host-targeted interventions for infection control.

In conclusion, our findings demonstrate that substrate type modulates multiple aspects of U2OS cell behavior, including morphology, cytoskeletal arrangement, mechanical properties, and microparticle uptake. These results underscore the mechanosensitive nature of osteosarcoma cells and highlight novel roles for microtubule cup-like structures and MAPs, particularly IQGAP1 in cellular uptake mechanisms.

These findings demonstrate that BPF-induced MARK2 upregulation activates EMT signaling, promoting malignant phenotypes, including proliferation, migration, and ferroptosis suppression, in lung cancer cells. The dual role of MARK2 as a prognostic indicator and actionable target in BPF-driven carcinogenesis offers new perspectives on environmentally triggered lung cancer pathogenesis and precision therapeutic approaches.

Particularly, compound 21 also exhibited superior activities in inducing the early apoptosis of HT29 cells and blocking the cell cycle in the G2 phase than the chemotherapeutic agent cisplatin...Compound 21, which prevented tumor cell metastasis and induced tumor cell apoptosis, exhibited potent antitumor activity in a zebrafish tumor model with xenografted HT29 cells. Furthermore, the histopathological evaluation demonstrated the ability of compound 21 to reduce the proliferation and improve the atypia of tumor cells in the abdominal cavity of zebrafish.

This study provides new insights into the pathogenesis of IBD by elucidating the role of microtubules in epithelial barrier disruption. Our findings propose microtubule-modulating therapeutics as a potential novel treatment strategy for IBD, highlighting the importance of stabilizing microtubules to restore epithelial integrity and reduce inflammation.

This interaction is critical for anchoring microtubules to the Golgi during cell migration, altering microtubule polarity distribution, and aiding Golgi reorientation. Our study reveals an important signaling pathway in Golgi reorientation during cell migration, which can provide insights for research in cancer cell migration, immune response, and targeted drug development.

These findings highlight the potential of urinary exosomal mRNA profiling, particularly focusing on RAB5B and WWP1, as a valuable strategy for improving the early detection of PCa.

To simulate targeting of MARK2/3, we adapted the CagA protein from H. pylori as a catalytic inhibitor of MARK2/3, which we show can regress established tumors in vivo. Together, these findings reveal MARK2/3 as powerful co-dependencies of YAP/TAZ in human cancer; targets that may allow for pharmacology that restores Hippo pathway-mediated tumor suppression.

Our study provides the first comprehensive evidence that m6A-modified circMARK2 contributes to WT progression by enhancing LIN28B mRNA stability, promoting cellular aggressiveness. CircMARK2 emerges as a potential biomarker for prognosis and a promising target for therapeutic intervention in WT, underscoring the clinical relevance of m6A modification in pediatric renal cancer.

Our study identified three CpG sites associated with PUFA intake. The mechanisms of these sites remain largely unexplored, highlighting the novelty of our findings. Further research is essential to understand the links between CpG site methylation and PUFA outcomes.

In this review, we aim to present detailed information on the structural features of MARK2 and its role in various signaling pathways associated with cancer and neurodegenerative diseases. Additionally, we further characterize the therapeutic potential of MARK2 in neurodegenerative diseases and cancer, and hope to facilitate basic research on MARK2 and the development of inhibitors targeting MARK2.