MYO6 (Myosin VI)

Molecular docking identified Deoxyuridine Monophosphate as a high-affinity inhibitor of TYMS. Our findings demonstrate that targeting thymidylate synthase enhances CD8 + T-cell infiltration and inhibits tumor growth in cervical cancer, establishing TYMS as a promising therapeutic target.

Furthermore, reporter gene analysis and proliferation assays supported a critical role for Myosin VI in AR signaling. Our findings thus uncover Myosin VI as an essential regulator for the spatial organization of androgen-dependent transcription.

In conclusion, the risk scores constructed from seven TRGs have great potential for survival prognosis, immunotherapy response and drug sensitivity. MYO6 plays an oncogenic role in promoting proliferation and metastasis in patients with LUAD, which provides a new theoretical basis for the diagnosis and treatment of LUAD patients.

MYO6 promoted CRC cell tumorigenesis and macrophage M2 polarization, and the mechanism was associated with USP7-induced MYO6 deubiquitination. These results suggested new targets for the development of epigenetic-based therapy in CRC.

CTSH overexpression or PTGES3 knockdown induced necroptosis and improved anti-PD1 therapy efficiency in syngeneic cancer mouse models. These findings indicate necroptosis genes as potential therapeutic targets in cancer treatments.

Clinically, higher levels of tumor spermidine and expression of methionine-to-spermidine metabolism-related gene signature predict poorer survival. Conclusively, our research identifies an unrecognized mechanism of pyroptotic resistance mediated by methionine-spermidine metabolic axis, providing a fresh angle for cancer treatment.

Additionally, we identified 11 differentially expressed genes that could provide insights into the potential mechanisms of immune escape in patients with lung cancer. These findings offer promising molecular targets for the detection and treatment of immune escape in clinical settings.

MYO6 has pro-tumor and Enz-resistant effects in CRPC, suggesting that targeting MYO6 may be beneficial for ENZ-resistant CRPC therapy through the AR/MYO6/FAK signaling pathway.

Furthermore, we have demonstrated that decreased MYO6 protein leads to reduced expression of GIPC1, SEPT2, and SEPT7 in breast cancer cells. These findings contribute to a more comprehensive understanding of the pathways influencing breast cancer cell migration, a critical aspect of metastasis.

Circ_0000395 promoted CRC cell growth, metastasis and oxaliplatin resistance via the miR-153-5p/MYO6 axis, which might provide new insights into the treatment of CRC.

In summary, this is the first study to report that miR-145-5p may inhibit EMT by targeting MYO6 in prostate cancer cells. The findings suggest miR-145-5p could be a useful diagnostic and prognostic biomarker for prostate cancer.

Furthermore, we found that microtubules may improve the stability and lifespan of B-lymphoma-cell NTs, while F-actin strengthens NTs by providing a structural framework for them. Our results may contribute to a better understanding of the regulation of the major cells of humoral immune response to infections.