ULK2 (Unc-51 Like Autophagy Activating Kinase 2)

Moreover, c-Jun overexpression counteracted the chemosensitivity and glycolytic suppression induced by the ectopic ULK2 expression in ovarian cancer.ConclusionsULK2 overcomes cisplatin resistance in ovarian cancer by downregulating glycolysis, a process mediated by phosphorylation-induced c-Jun degradation. These findings emphasized the role of ULK2 as a tumor suppressor, offering novel insights for chemotherapy in ovarian cancer.

Furthermore, ULK2 was found to upregulate MCT4 expression on the plasma membrane, resulting in increased extracellular lactate levels and enhanced invasive capacity in vitro. These findings identify ULK2 as a contributing factor to CRC invasion and highlight its therapeutic potential for suppressing tumor aggressiveness.

Although autophagy typically acts as a cytoprotective mechanism, in this context, the autophagy-dependent degradation of BCR::ABL induced cell death. These findings reveal a novel regulatory axis involving ULK2, FIP200, AMPK, and autophagy, suggesting a unique role for ULK2 in CML pathophysiology and offering potential therapeutic insights.

We demonstrated that CD14+ monocytes from MM can disrupt the delivery of antigenic peptides through the antigen processing and presentation pathway. This disruption affects T-lymphocytes activity and attenuates their ability to kill malignant cells and secrete cytokines. These findings lay the foundation for understanding the immuno-suppressive environment in MM, improving the efficacy of immunotherapy based on T-lymphocytes, and developing new therapeutic targets.

Finally, our results indicated that ANRIL overexpression facilitated Y79 cell proliferation and cisplatin-induced apoptosis. Our results indicated that ANRIL promoted the proliferation and cisplatin resistance of Y79 cells through activating autophagy by promoting TSC1/ULK2 ex- pression via acting as a miR-328-3p sponge.

The low ULK2, UVRAG, and miR-374 expression group exhibited significantly poor overall survival in glioma, while miR-21 over-expression indicated a poor prognosis in glioma patients, validating it in our population. This study provides comprehensive insights into the molecular landscape of gliomas, highlighting the dysregulation of autophagy genes ULK2, and UVRAG and the associated miR-21, miR-126 and miR-374 as potential prognostic biomarkers and emphasizing their unique significance in shaping survival outcomes in gliomas within the specific context of the Pakistani population.

This study provides comprehensive insights into the molecular landscape of gliomas, highlighting the dysregulation of autophagy genes ULK2, and UVRAG and the associated miR-21, miR-126 and miR-374 as potential prognostic biomarkers and emphasizing their unique significance in shaping survival outcomes in gliomas patients.

In summary, the collective data indicated that ULK2 acted as a tumor suppressor in ovarian cancer by upregulating the expression of IGFBP3. Our study underscores the potential utility of ULK2 as a valuable prognostic marker for ovarian cancer.

Furthermore, chloroquine (an autophagy inhibitor) sensitized SORE6 but not SORE6 cells to Ara-C...MRT68921 significantly sensitized SORE6 but not SORE6 cells to Ara-C...Lastly, using pretreatment and relapsed AML patient bone marrow samples, we found that ULK2 expression was higher in relapsed AML. To conclude, our results supported the importance of autophagy in the relapse of FLT3-mutated AML and highlighted ULK2 in this context.

DβH, UBE2D3, SOD1, UBE2D1, and LOXL2 are potential candidates implicated in LUAD and can be further explored for their application as diagnostic, prognostic, and therapeutic biomarkers for LUAD.