CDC25C (Cell Division Cycle 25C)

Knockdown of PRPF4B triggers ROS-dependent DNA damage, cell cycle arrest, and suppression of HCC proliferation, while enhancing sorafenib sensitivity via inhibition of the NF-κB pathway. Therefore, PPRF4B may be a potential therapeutic target for HCC treatment and sorafenib sensitization.

Importantly, genetic or pharmacological disruption of this GPRIN1-CDK1-PI3K/Akt axis completely abrogated tumorigenesis in vitro and in vivo. Taken together, these results reveal GPRIN1 as a master regulator whose dual transcriptional and post-translational control of CDK1 integrates cell cycle progression with mitochondrial homeostasis, suggesting that targeting GPRIN1 may represent a highly specific therapeutic strategy in this lethal malignancy.

The results demonstrate that isoliensinine induces apoptosis in OSCC cells via ROS-mediated mitochondrial pathways and cell cycle arrest, a process associated with MAPK signaling pathway activation. Transcriptome analysis further revealed that isoliensinine modulates multiple miRNAs that target the MAPK pathway, suggesting that miRNA regulation may mediate its activation of MAPK signaling.

Immune infiltration analysis further suggested that CDC25C, CDK2, and KIF11 may modulate the infiltration of B cells, CD8⁺ T cells, and macrophages, implying that Bisphenols-induced molecular perturbations could impact the tumor microenvironment. This study provides a reference for further exploration of the links between environmental exposures and cervical cancer development and lays a foundation for mechanistic investigations.

A CRC risk model based on 6 AS-related genes was developed, identifying 3 novel AS genes. It highlights shared genetic factors, offering prognostic biomarkers for both diseases and insights into their interconnected mechanisms.

Given their unique properties and clinical relevance, PGCCs represent a promising frontier in cancer biology with the potential to overcome therapeutic resistance and prevent tumor recurrence through targeted interventions. This review seeks to elucidate the role of PGCCs across multiple cancer types and highlights their emerging potential as novel targets for future cancer therapies.

A competing endogenous RNA (ceRNA) network involving miRNAs (e.g., miR-16-5p, miR-126-5p) and lncRNAs (e.g., AC008124.1, AC064799.2, AGAP11) potentially modulates their expression. This study identifies seven novel candidate biomarkers dysregulated in endothelial cells under combined BCR-ABL and exosomal stimulation, shedding light on the molecular crosstalk between leukemic cells and the vascular niche.

Collectively, the present study establishes the potential of Houttuynia cordata-derived exosome-like nanovesicles as a natural therapeutic platform against TNBC, with macrophage membrane coating further augmenting their efficacy through biomimetic targeting. MCELNs may represent a promising drug delivery strategy for enhancing treatment efficacy while minimizing systemic toxicity in breast cancer therapy.

This signature highlights the clinical relevance of OXPHOS in LUSC prognosis and may guide personalized therapeutic strategies targeting metabolic vulnerabilities. Study limitations include its retrospective design and lack of experimental validation.

These findings indicate that γT3 and δT3 inhibit HCC2998 cell proliferation by activating the DDR pathway, highlighting their potential as therapeutic agents to overcome cell cycle arrest resistance in CRC. This study provides critical insights into the molecular actions of γT3 and δT3, supporting their further investigation as promising candidates for CRC intervention.

Notably, efficacy was validated in colorectal cancer patient-derived organoids, providing clinically relevant insights into patient-specific responses. Together, these findings define a new class of CDC25 inhibitors with potent and selective anticancer activity, advancing prospects for next-generation therapeutics in leukemia and colorectal cancer.