SLC16A3 (Solute Carrier Family 16 Member 3)

Additionally, SLC16A3 downregulation reduced cisplatin sensitivity in LUAD cells. Our study highlights the clinical translational potential of a five-gene zinc homeostasis network signature in predicting prognosis and guiding personalized therapeutic strategies for LUAD.

By targeting these transporters with small molecule inhibitors, it may be possible to disrupt essential metabolic pathways in cancer cells, thereby enhancing treatment efficacy and improving patient outcomes. This research establishes a foundation for the development of SLC-targeted therapies in precision oncology, aiming to improve survival rates for patients with OV.

Silencing SLC16A3 significantly reduced cell survival and promoted caspase-3-dependent apoptosis, which was further enhanced by ionizing radiation or cisplatin treatment. Phospho-kinase array profiling demonstrated activation of the p38-MAPK pathway upon SLC16A3 inhibition, and pharmacological blockade of p38 (SB203580) attenuated apoptosis, confirming that SLC16A3 knockdown-induced apoptosis is p38-dependent. Collectively, these findings uncover a previously unrecognized SLC16A3-p38-caspase signaling axis that promotes therapeutic resistance and highlight SLC16A3 as a promising therapeutic target for overcoming radioresistance and chemoresistance in lung cancer.

SLC16A3 in LUAD modulates the glycolysis pathway to facilitate M2 polarization of macrophages.

Key lactylation-related genes, including LDHA and SLC16A3, were associated with immune exhaustion and cisplatin resistance...Perturbation sensitivity and repurposing analyses revealed novel therapeutic vulnerabilities. This study establishes a precision oncology framework that integrates lactylation biology with AI-driven analytics to uncover druggable targets, enhance patient stratification, and inform the design of multi-target therapies in ovarian cancer.

Thus, BMI1 expression leads to increases in key features of early-stage, carcinogen-induced tumorigenesis, including metabolic reprogramming. Consequently, limiting BMI1 could be a potential target for cancer prevention approaches that merits further consideration and additional functional studies.

Alone or combined with inhibition of mitochondrial respiration by metformin and phenformin, the MCT4 inhibitor syrosingopine significantly inhibits lactate efflux, induces cell viability reduction in four different RCC cell lines and patient-derived 2D/3D models, and alterations in cellular metabolism and mitochondrial respiration. Six patient-derived RCC air-liquid interface models, mimicking the complex RCC architecture, corroborate these data. Beyond potential prediction of patient outcome using MCT4 expression and DNA methylation at specific CpG sites, drug targeting of MCT4 and inhibiting mitochondrial respiration synergistically is a novel treatment strategy for metastatic ccRCC.

Multivariate Cox analysis confirmed that the risk signature provided independent predictive information from clinical variables. In conclusion, the risk signature accurately identifies breast cancer patients at risk of lung metastasis, enabling clinicians to better assess risk and tailor treatment strategies effectively.

Our findings reveal that the HIF1A-SLC16A3-lactate axis orchestrates ferroptosis suppression and therapeutic resistance in LUAD. Targeting SLC16A3 represents a promising metabolic strategy for overcoming EGFR-TKI resistance by reactivating ferroptosis.

Tissue microarrays analysis suggested that CBX6 and SMARCD1 were linked to immunosuppression and poor prognosis in clinical samples. In conclusion, this study suggests that CBX6 induces CD8+ T cell exhaustion and tumor development in ESCC through SMARCD1-mediated CCL8 secretion and lactate efflux.

However, it demonstrates a declining trend in the progression of CRC from stage I to IV, which may be intricately associated with the metastasis of CRC. The WARS1 can serve as a reliable indicator of the immune response in CRC, thereby demonstrating its potential to impede tumorigenesis or metastasis.

We established a DMA analysis pipeline linking the gene dependencies of breast cancer cell lines to multi-omics characteristics, thus elucidating the underpinnings of tumor dependencies and offering a valuable resource for developing novel precision treatment strategies incorporating relevant markers.