MYC (V-myc avian myelocytomatosis viral oncogene homolog)

These results demonstrate that partial depletion of SART1 preferentially induces spindle defects and cell death in transformed cells. Given that complete loss of SART1 is incompatible with normal development, our findings suggest that transient or partial inhibition of SART1 may provide a basis for selectively eliminating transformed cells while sparing normal cells.

It delves into its regulation of core cellular processes, its integration into oncogenic signaling networks, and its recently discovered functions in epigenetic and metabolic reprogramming. By consolidating this knowledge, we aim to highlight the multifaceted nature of DHX33 in cancer biology and firmly establish its potential as a viable and promising therapeutic target for future anticancer strategies.

Critically, Ctnnb1 silencing in T cells abrogated the enhanced proliferation, TCM formation, and cytotoxic activity induced by SHP1-deficient DCs. DC-intrinsic SHP1 restrains central memory CD8+ T cell formation via the TCF-1/Wnt/β-catenin axis.

Recent clinical progress with Omomyc-derived OMO-103 and other MYC-network-targeting agents supports the feasibility of therapeutically intercepting this historically challenging pathway. However, because many MYC-directed strategies affect essential transcriptional, chromatin, and metabolic programs, future development will require careful biomarker selection, rational combinations, and rigorous evaluation of therapeutic windows. By integrating mechanistic and translational literature, this review highlights MYC as a dynamic cancer dependency and discusses opportunities for precision intervention.

MTT and colony formation assays identified compound 1 as the most potent antiproliferative agent, with an IC50 of 6.53 μM in MCF-7 cells, which outperformed tamoxifen under identical experimental conditions...Taken together, these observations establish compound 1 as a promising antitumor lead scaffold for subsequent structural modification. Further investigations regarding its selectivity profile, systemic toxicity, pharmacokinetic properties, and in vivo therapeutic efficacy are therefore warranted.

Subsequent studies using a small molecule Wnt inhibitor in SMARCA4-deficient cells and thoracic SMARCA4-UT patient-derived organoids demonstrated induction of apoptosis, inhibition of cell stemness, and suppression of tumor cell growth. These results suggest the potential for developing a novel therapeutic strategy targeting cancer stem cells for the treatment of thoracic SMARCA4-UT.

Understanding its histological features and immunohistochemical profile facilitates its diagnosis and differential diagnosis, including CK20 positivity and Ki-67 negativity in the superficial layer, and high Ki-67 expression with negative CK20 staining in the deep layer. KRAS gene mutation is also an important diagnostic feature.

In a xenograft model, CDC20 knockdown reduced tumor growth, whereas its overexpression enhanced tumor progression. These findings suggest that CDC20 contributes to prostate cancer progression, at least in part, through a c-MYC-associated PI3K-AKT signaling axis, and support its potential relevance for prognostic assessment and therapeutic targeting.

P2, N=286, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027

Representative examples of the obtained compounds: phenazin-2-(10H)-one (5d), 2-aminophenazine derivatives (8b, 9a, and 10ba), and 2,3-dialkoxyphenazine (6a) were investigated for their interaction with the G-quadruplex formed by the DNA sequence derived from the NHE III1 promoter region of the c-MYC oncogene. Destabilization of the investigated DNA structure by all of the tested compounds was confirmed by UV-vis spectrophotometry and CD spectroscopy.

Binding free energy calculations confirm strong spontaneous binding (ΔGbind ≈ -44 to -47 kcal/mol), while residue-level decomposition and ASIE analysis precisely identify core anchoring hotspots (Phe370, Tyr643, His592, His261). Collectively, this study reveals that CAS-010 achieves potent inhibition not by global rigidification, but through orchestrated dynamic remodeling of USP28, providing a theoretical framework and structural guidance for rational design of next-generation USP28 inhibitors.

LMSCC16 also harbored two TP53 mutations and showed increased resistance to Cisplatin and Paclitaxel compared to established TSCC cell lines. In contrast, LMSCC16 showed significant modulation of OCT4, increased CCND1 and CCNB1 expression, and reduced CDH1 levels following treatment. We established two novel TSCC cell lines that represent clinically relevant models to explore TSCC carcinogenesis and therapeutic responses, particularly in non-smoking populations.