Prostate Cancer

Microscopic observations demonstrated that lung cancer cells successfully metastasize to bone stroma and disrupt the bone microenvironment, like the in vivo effect. ELISA and qRT-PCR analyses also demonstrated an increase in associated mesenchymal cytokines and genes. Furthermore, an increase in epithelial genes related to proliferation was observed in the lung chamber. ELISA analysis also revealed an increase in epithelial genes. All analyses show that lung cancer cells successfully metastasized to the bone chamber, highlighting the physiological relevance of our platform in simulating in vivo metastatic behavior. It's interesting to note that the lung chamber's parallel upregulation of markers of epithelial proliferation points to a spatially separate but biologically related dynamic where primary tumor dissemination and secondary site colonization take place simultaneously.11 The lung cancer metastasis-on-a-chip platform can be adapted to study how a broad range of exposome factors, such as environmental pollutants, dietary components, and lifestyle-related exposures, affect cancer progression and metastasis in besides modeling tumor-bone interactions.12 his system, similar to our previous airway epithelial barrier-on-a-chip work, could bring exposome research into oncology, providing a versatile bridge between cancer biology, toxicology, and regulatory science (Figure 1).13 This helps to remove animal testing worldwide and advances precision medicine and cancer prevention.

Key markers such as miR-141, miR-375, and PCA3 showed strong diagnostic and risk stratification value in PCa. This non-invasive approach holds promise for improving early detection and clinical risk assessment.

P=N/A, N=90, Recruiting, Vejle Hospital | Not yet recruiting --> Recruiting

P=N/A, N=100, Suspended, University of Arizona | Trial completion date: Sep 2027 --> Nov 2028 | Trial primary completion date: Sep 2026 --> Nov 2027

P2, N=58, Active, not recruiting, OHSU Knight Cancer Institute | Trial completion date: Jun 2025 --> Jun 2026

P=N/A, N=600, Completed, Wake Forest University Health Sciences | Active, not recruiting --> Completed

P=N/A, N=852, Active, not recruiting, ECOG-ACRIN Cancer Research Group | Trial completion date: Dec 2025 --> Aug 2026 | Trial primary completion date: Dec 2025 --> Aug 2026

P1, N=80, Recruiting, ARTBIO Inc. | Trial completion date: Sep 2033 --> Nov 2028

Our study demonstrates that CHD1L is markedly upregulated in prostate cancer and contributes to tumor progression. Pharmacological inhibition of CHD1L with the selective inhibitor OTI-611 significantly suppresses proliferation, migration, and invasion, while inducing apoptosis in vitro and in vivo. Mechanistically, these effects are mediated through activation of the FOXO3-PUMA axis, as FOXO3 suppression abrogates OTI-611-induced apoptosis. Moreover, OTI-611 exhibits strong synergy with docetaxel, enhancing apoptotic cell death and providing a potential strategy to improve therapeutic efficacy in prostate cancer.

AA induces ER stress, leading to transcriptional downregulation of the AR and suppression of PCa cell viability and proliferation. Targeting the PERK pathway may enhance AA efficacy in AR-driven PCa.

In this study, we propose that an AREG-based signature comprising ACSM3, ACTG2, and DES effectively predicts prognosis and reflects immune microenvironment characteristics in PRAD. Through systematic analysis, we established a prognostic model utilizing these three AREGs, which demonstrates strong potential as a clinical predictor for PRAD patient outcomes.

LNCaP and VCaP cells were treated with enzalutamide (0.1-10 µM) for 1-7 days...Crucially, ER stress markers correlated with PSMA trafficking, suggesting serum-based profiling could enable individualized ARB adjustments. Future studies should validate these biomarkers to establish personalized ARB-RLT strategies for improved clinical outcomes.