CDC25A (Cell Division Cycle 25A)

CDC25A is an independent prognostic biomarker of clinical outcome in breast cancer. Further functional studies are warranted to validate CDC25A as a potential prognostic and therapeutic biomarker in breast cancer.

Parabens may promote HNSCC progression by disrupting cell cycle regulation and immune responses via direct interactions with key hub genes. These findings provide a novel mechanistic basis for the carcinogenic potential of parabens in HNSCC and underscore the need for further experimental and epidemiological validation.

Moreover, Western blot and immunofluorescence results demonstrated that diosgenin inhibited migration by suppressing epithelial-mesenchymal transition(EMT) and the RhoA-ROCK1 signaling pathway. In conclusion, diosgenin induces G_0/G_1 phase arrest in MDA-MB-231 cells by regulating cell cycle-related proteins and significantly inhibits cell migration by suppressing F-actin formation, reducing filopodia on the cell surface, and inhibiting EMT and the RhoA-ROCK1 pathway.

This is the first report of C8-HSL as a promoter of lung cancer cell proliferation, migration, and invasion. Taken together, C8-HSL is a potential risk factor for lung cancer, and strategies targeting C8-HSL-producing bacteria and monitoring C8-HSL concentrations may be beneficial for the prevention and control of lung cancer.

INSM1 overexpression in SH-SY-5Y cells upregulated neuroendocrine and thyroid hormone-related genes (CHGA, CHGB, DDC, NCAM1, DIO3, TH), while suppressing genes involved in cell cycle (RRM, CDC25A), methionine metabolism (AHCY, MAT2A), transcriptional regulation (MYBL2, EZH2), and oncogenic signaling (ALK, LINC011667). These findings suggest that INSM1 promotes NB aggressiveness by sustaining a neuroendocrine progenitor-like phenotype through metabolic-epigenetic coupling.

Mechanistically, D3 exerts antitumor effects by degrading the target protein Cdc25, upregulating p-CDK1/2 levels, and subsequently inducing G2/M phase cell cycle arrest and apoptosis. This study validates PROTACs as a breakthrough strategy to target "undruggable" Cdc25, provides a novel quinoline-dione-based scaffold for antitumor drug development, and offers a rational design paradigm for tackling intractable phosphatase targets.

In conclusion, our findings suggest that the USP1/CDC25A/CDK1 axis influences esophageal carcinogenesis and progression. The online version contains supplementary material available at 10.1007/s13205-025-04663-1.

Paeoniflorin induces melanoma cell senescence through the ER stress/calpain1/ERK5/p27 signaling axis, suggesting its potential as a novel therapeutic strategy against SKCM.

Modulating the miR-122-5p/CDC25A axis may provide potential molecular targets for inhibiting CML progression through regulation of cell cycle pathways. Findings are exploratory and based on bioinformatics with limited in vitro expression confirmation; functional studies are required to establish causality.

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.

The combined use of palbociclib and PIK75 synergistically inhibited the expression of the cell cycle proteins CCNE1, CDC6, and CDC25A, as well as the abnormal activation of PIK3CA and AKT phosphorylation. The combination of these two drugs synergistically inhibited tumor cell cycle progression and promoted apoptosis in vitro and in vivo, which provides a promising idea for the treatment of ESCC in the future.