CYP17A1 (Cytochrome P450 Family 17 Subfamily A Member 1)

RAMRGs serve as useful biomarkers to predict prognosis in LUAD patients, and may guide the immunotherapy regimen.

CYP51A1 knockout suppressed androgen-regulated genes in vitro and in vivo in prostate cancer xenografts. These findings have broad implications for sex steroid physiology and pharmacologic therapies for steroid-dependent diseases.

This study confirmed the validity of the cyclophosphamide-busulfan induced mouse model of ovarian senescence, highlighted both the shared and distinct molecular mechanisms of physiological and pathological ovarian aging, and identified promising early biomarkers and therapeutic intervention targets.

These components are known to exert therapeutic effects against lung cancer by targeting CYP17A1, CYP19A1, and AR, as well as by modulating pathways such as EGFR tyrosine kinase inhibitor resistance and prostate cancer. This study successfully establishes an eco-efficient extraction method for naringin and clarifies the multi-target mechanism of action of CGT extracts against lung cancer.

These findings suggest a possible role for these polymorphisms in ovarian cancer risk and highlight the need for further studies. This review was registered in PROSPERO (CRD42023464116).

Additionally, extended 200 ns molecular dynamics simulations further validated the complexes, revealing stable RMSD, reduced SASA, favorable hydrogen bonding, and strong MM-GBSA binding free energies (△G_bind = -42.6 kcal·mol-1 for sarcorine C vs -40.8 kcal·mol-1 for roscovitine). These findings establish S. saligna as a promising source of anticancer steroidal alkaloids and report, for the first time, the selective cytotoxic activity of sarcorine C and salonine C against colon cancer cells, supported by integrated experimental and computational evidence.

No significant associations were found between polymorphisms in CYP17A1, HSD3B1 and TT levels. The HSD3B1 CA genotype showed a non-significant trend toward increased PCa risk (OR = 2.39, p = 0.183) that requires validation in larger studies before any clinical relevance can be established.

Our study investigated the hub genes and underlying mechanisms of BDCPP-induced EC. The findings not only offer novel insights into the role of environmental pollutants in EC development but also present an analytical framework for elucidating the carcinogenic mechanisms of other environmental chemicals.

The molecular docking results revealed the ability of both n-hexadecanoic acid and L-carnitine to activate SIRT1 and subsequent antioxidant, anti-inflammatory, and anti-apoptotic pathways. This ovoprotective effect is suggested to be mediated through activation of different SIRT1-mediated protective signaling pathways that remodel ovarian redox status, inflammation, and apoptosis, which may strengthen the potential role of SP and L-car as a chemotherapy adjuvant, reducing the negative health effects of early menopause after cancer therapy.

The observed deeper energy wells in diffusion maps indicate stronger binding affinities and reduced conformational transitions compared to reference inhibitors, such as abiraterone and acetazolamide. These computational insights align with experimental findings, suggesting that 6d holds significant promise as a potent dual-target inhibitor with applications in prostate cancer therapy and glaucoma treatment.

These findings collectively indicate that chronic low-dose DBP exposure induces transgenerational reproductive impairment through endocrine disruption and oxidative stress mechanisms, progressively compromising ovarian function and fertility across generations via HPO axis dysregulation. The study provides critical evidence for multigenerational reproductive risk associated with environmental phthalate exposure.

Given the therapeutic potential of ERα degradation in overcoming endocrine resistance, we investigate the inhibitory effect of Bufalin on endocrine-resistant models and prove Bufalin reverses Tamoxifen resistance in vitro, in vivo, and in patient-derived breast cancer organoids from tamoxifen-relapsed cases. Collectively, our findings indicate that Bufalin functions as a molecular glue to degrade ERα, offering a potential therapeutic strategy for reversing Tamoxifen resistance.