Cervical cancer is the fourth leading cause of cancer mortality in women worldwide, with limited therapeutic options for advanced or recurrent cases. In this study, the effects of a recent thieno[2,3-b]pyridine derivative, (E)-3-amino-5-(3-bromophenyl)acryloyl)-N-(3-chloro-2-methylphenyl)-6-methylthieno[2,3-b]pyridine-2-carboxamide (compound 1), on two cervical cancer cell lines, HeLa and SiHa, are investigated. Cytotoxicity was assessed by MTT assay, apoptosis rates were measured by flow cytometry, and metabolic profiling was performed by GC-MS. The study also examined the expression of eight glycosphingolipids (GSLs) in cancer stem cells (CSCs) and non-CSCs to assess glycophenotypic changes. Compound 1 showed significant cytotoxicity in both cell lines, with apoptosis identified as the primary mechanism of cell death. A significant reduction in the CSC population was observed, particularly in the SiHa cell line. Compound 1 treatment altered GSL expression and decreased GM2 levels in both CSCs and non-CSCs in the SiHa cell line and Gg3Cer levels in the HeLa cell line. Metabolic profiling identified 23 and 21 metabolites in the HeLa and SiHa cell lines, respectively, with significant differences in metabolite expression after treatment. These results underscore the potential of compound 1 as a promising therapeutic candidate for cervical cancer and warrant further investigation in preclinical and clinical settings.

Epidemiological studies suggest that, despite the adverse effects of excessive alcohol intake, low-to-moderate levels of wine consumption have been associated with favorable cardiovascular outcomes. While the biological effects of polyphenol-rich red wine have been extensively studied, less is known about the impact of white wine on myocardial cellular function and the underlying mechanisms. In this study, young male Sprague-Dawley rats were given ad libitum access to white wine or water for four weeks, after which cardiac mitochondrial function, cardiomyocyte susceptibility to oxidative stress, and cardiac transcriptomic profiles were assessed using respirometry, ROS measurements, in vitro oxidative stress assay, and RNA sequencing. White wine consumption did not significantly alter mitochondrial respiratory capacity, expression of antioxidant enzymes or cardiomyocyte survival following oxidative challenge. However, mitochondrial ROS production at respiratory complex I was significantly reduced, particularly during reverse electron transport mimicking ischemia/reperfusion. Transcriptomic analysis revealed modest changes, with no genes meeting the false discovery rate threshold. Analyses based on nominal significance revealed changes associated with mitochondrial electron transfer, protein quality control, apoptosis, and inflammatory signaling. In conclusion, four-week white wine consumption was associated with reduced mitochondrial ROS without impairing cardiac bioenergetics, accompanied by subtle transcriptional responses.