MAD2L1 (Mitotic Arrest Deficient 2 Like 1)

In vitro, CCNB1 knockdown triggered cell cycle arrest, thereby suppressing the proliferation of colorectal cancer cells. This study validated CCNB1 as a dual-purpose biomarker for CRC diagnosis and favorable prognosis, highlighting its potential utility in clinical management.

This study systematically delineates a novel panel of early-detection biomarkers for CRC and identifies SB-225002 as a repurposed candidate therapeutic agent. The integrative strategy combining multi-cohort transcriptomic analysis, drug-repositioning platforms, molecular docking, and experimental validation offers a feasible framework for discovering clinically actionable biomarkers and small-molecule therapies for CRC.

The findings of the present study provided a set of four key genes with valid clinical utility that can serve as an alternative tool for prognosis and identification of new targets in CRC treatment.

The robust association between CDK1 expression, tumor grade and survival, coupled with functional validation across complementary assays, positions CDK1 inhibition as a promising therapeutic strategy. The mechanistic elucidation of its cell cycle network provides a novel framework for targeting glioma‑specific therapeutic targets..

Additionally, we explore the potential of targeting these molecules to enhance the efficacy of radiation therapy and improve patient outcomes. Our study contributes to the comprehension of the molecular processes underlying oral cancer and provides insights into the development of novel therapeutic strategies based on personalized medicine.

Collectively, our study identifies MAD2L1 as a promising oncogenic biomarker and therapeutic target in OSCC, whose upregulation drives tumor progression, impairs patient prognosis, and disrupts m6A modification.

9 core genes (CCNB1, CCNB2, MAD2L1, BUB1, TTK, CDC20, AURKA, RRM2, GTSE1) were obtained through the KEGG pathway enrichment, which mainly enriched in 4 pathways, namely, Cell cycle, Oocyte meiosis, p53 signaling pathway, and Progesterone-mediated oocyte maturation, respectively. Nine critical dependable DEGs were identified in limited-stage NSCLC using integrated bioinformatical approaches, and these core genes show great potential as prospective biomarkers and therapeutic targets in the progression of limited-stage NSCLC. non-small cell lung cancer, biomarkers, therapeutic targets, p53 signaling pathway, bioinformatics analysis.

These genes likely mediate their effects by influencing immune cell infiltration, participating in immune regulation, and modulating inflammatory responses. Our findings offer new insights into drug selection and immunotherapeutic strategies for SS.

Notably, LZU-WZLYCS01 shows superior antitumor efficacy to gemcitabine-cisplatin (GC) chemotherapy and maintains significant activity in GC-resistant PDX models. These findings present a promising therapeutic candidate for targeted bladder cancer treatment.

Furthermore, we found that inhibiting the apoptosis-related gene CTTN suppresses the anti-apoptotic capacity of HNSCC. Results from HNSCC-PDOs suggest that CTTN may represent a key target for HNSCC invasion and treatment.

The model outperforms established clinical factors in predicting NB outcomes and provides added clinical decision-making value. Further prospective validation and mechanistic investigations may facilitate the translation of this prognostic signature into routine clinical practice, enabling more refined risk stratification and personalized treatment strategies for children with NB.