CCND1 (Cyclin D1)

In conclusion, our findings suggest that c-Myc overexpression and MYC rearrangement are associated with ibrutinib resistance in MCL. Detecting MYC rearrangement in selected MCL cases could be critical for optimizing treatment strategies and improving patient outcomes.

Early clinical data demonstrated activity of BLU-222, a potent and selective CDK2 inhibitor, both as monotherapy (CCNE1 amplified) and in combination with ribociclib and fulvestrant in patients with HR+/HER2- breast cancer. These findings provide evidence that CDK2i combined with CDK4/6i can address multiple known mechanisms of resistance to CDK4/6i, enhancing antitumor responses in preclinical breast cancer models.

Critically, targeted knockdown of STEAP3 remarkably inhibited TNBC cells proliferation, migration and xenograft tumor growth. These findings unveil a critical pro-tumorigenic copper-driven pathway-distinct from cuproptosis-operating through STEAP3/copper/CDK16/JAK1 axis, and highlight STEAP3 as a promising therapeutic target for TNBC.

Furthermore, exploratory molecular docking was also performed to probe possible binding modes of 4a with PI3Kα, STAT3, and Cyclin D1. Collectively, these findings indicate that C-3 glycosylation of kidjoranin may represent a viable approach for developing new anticancer candidates.

DDX10 contributes to the proliferation and invasion of DLBCL cells via positively regulating FBL, highlighting the DDX10-FBL axis as a potential therapeutic target. This work provides new insights into DLBCL pathogenesis and underscores the biomedical relevance of targeting DDX10-FBL.

Docking studies confirmed their interaction with the colchicine-binding site of tubulin. Together, the results support further investigation of these compounds as microtubule-interacting agents with selective antiproliferative activity.

This study demonstrated that GPX8 is a critical oncogene in OS progression and that its expression is regulated by KLF16. Targeting the KLF16/GPX8 axis may offer promising prospects for the development of novel therapeutic strategies against OS.

Notably, miR-34 mimics have demonstrated potential in tumor trials to restore tumor suppressor functions, offering the promising and novel strategies for combined anti-viral and anti-tumor therapies. In the future, through multi-omics integration, the development of novel nano-delivery systems, and multicenter clinical trials, miR-34 is expected to become a crucial target for viral prevention and precision tumor therapy.

ECT2 is identified as a potential pan-cancer prognostic biomarker with dual roles in tumor initiation and progression, as well as in modulating the tumor immune microenvironment. Our findings suggest that ECT2 may serve as a promising therapeutic target in cancer immunotherapy, warranting further investigation into its immune-regulatory and oncogenic functions.

This study's findings suggest that miR-100 can inhibit NSCLC progression by specifically targeting CDC25A, a cell cycle regulator, and its downstream molecular targets. Hence, miR-100 may have significant therapeutic potential against NSCLC.

Additionally, ORAOV1 expression correlated with enhanced infiltration of immunosuppressive cells, including regulatory T cells, myeloid-derived suppressor cells, and cancer-associated fibroblasts, as well as upregulation of immune checkpoint markers (PD-1, PD-L1, and CTLA-4). These results indicate that ORAOV1 may modulate the immunosuppressive tumor microenvironment and contribute to resistance against immunotherapy, highlighting its potential as a therapeutic target in HCC.