CDC7 (Cell Division Cycle 7)

TAK-931 treated prostate cancer cells exhibit an abnormal cell cycle profile, suggesting that CDC7 inhibition induces replication stress and promotes apoptosis. Collectively, our findings demonstrate that CDC7 is a regulator of tumor progression in prostate cancer and represents new therapeutic target in advanced prostate cancer.

Drug sensitivity profiling revealed subgroup-specific vulnerabilities: IT-8 to DNA damage checkpoint inhibitors, IT-21 to PLK/mTOR inhibitors and IT-13+22 to BRAF/EGFR-targeted agents. These findings highlight AML-IT heterogeneity and therapeutic potential.

While 5-fluorouracil (5-FU) and oxaliplatin remain the cornerstone of chemotherapy for KRAS-mutant CRC, their efficacy is frequently undermined by intrinsic and acquired resistance. Importantly, this work elucidated the subcellular distribution and proteostasis regulation of CDC7 under genotoxic stress, which is a switch for chemosensitivity in KRAS mutant CRC. These findings established CDC7 as a therapeutic vulnerability in KRAS-mutant CRC and provided a rationale for targeting CDC7 as a therapeutic strategy to restore chemosensitivity to 5-FU/oxaliplatin.

Moreover, TP53RK overexpression sensitized cells to DNA replication stress (aphidicolin) and CDC7 inhibition (XL413), highlighting its potential as a therapeutic strategy. These findings establish TP53RK as a pivotal regulator of DNA replication fidelity and genomic stability, thereby providing a promising therapeutic target for CRC.

DDR-targeting agents hold significant promise, especially when guided by predictive biomarkers and combined with other therapies. As these agents move into later-phase trials, future development should emphasize biomarker-driven design, toxicity mitigation through dose optimization, and expansion into non-canonical tumor types to maximize clinical impact.

© 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland

Consequently, we confirmed that HBc promotes the malignant progression of HCC by inducing the KCNQ1OT1/miR-335-5p/CDC7 axis. This axis may provide a novel and promising therapeutic target for improving malignant progression in HCC, particularly in patients with HBV infection.

Therefore, the CDC7-DBF4 complex may represent an attractive candidate therapeutic target for the treatment of cancers with miR-30a inactivation. Altogether, miRTARGET is a powerful and user-friendly web tool for exploring miRNA targets with therapeutic or prognostic potential in cancer.

especially in different clinical subtypes. In conclusion, DBF4B may be a key molecular biomarker for pan-cancer immunology and prognosis and an independent prognostic risk factor for LIHC.

In addition, changing the combination of DNA replication-related proteins used for discrimination resulted in a high accuracy (95-100 %). A discriminant analysis with NSVM using the LI and OD of DNA replication-related proteins may enable the differentiation of EA from its precursor lesions.

CTC gene expression provides information about treatment outcomes in HR + /HER2- metastatic BC patients receiving CDK4/6i plus ET and could guide personalized strategies and improve prognosis.

Chemotherapy for cancer frequently uses platinum-based medications, including oxaliplatin, carboplatin, and cisplatin; however, due to their high systemic toxicity, lack of selectivity, drug resistance, and other side effects, platinum-based medications have very limited clinical application. Excluded publications were works of low relevance, duplicates, or those with insufficient information. The mechanism of oxaliplatin's anticancer effect, oxaliplatin resistance and its amelioration, and the role of XL413 in oxaliplatin treatment were the main topics of the 140 publications that were ultimately included for analysis.