SLC16A4 (Solute Carrier Family 16 Member 4)

By simultaneously modulating metabolic pathways and immune responses, this strategy represents a novel integrative approach for HCC treatment. These results not only elucidate the molecular basis of CTD/Rg3 efficacy but also provide robust preclinical support for its clinical translation in HCC management.

We believe the mechanistic insights presented in this study contribute meaningfully to the understanding of CRC biology. We would like to share our interpretations and hope to further discuss with the authors certain unexplored aspects and potential connections in this area.

The MCT8 mAb treatment also enhanced the efficacy of anti-PD-L1 in mice bearing tumors. This study supports that SLC16A2 contributes to Tex cell accumulation in association with increased lactate uptake and hampers immune activity in HCC, supporting SLC16A2 as a promising target to enhance immune activity in HCC management.

The MCT8 mAb treatment also enhanced the efficacy of anti-PD-L1 in mice bearing tumors. This study supports that SLC16A2 contributes to Tex accumulation in association with increased lactate uptake and hampers immune activity in HCC, supporting SLC16A2 as a promising target to enhance immune activity in HCC management.

SLC16A4 exhibits cancer-specific expression patterns and plays a multifaceted role in tumor progression, metabolism, and immune regulation. Its potential as a diagnostic and prognostic biomarker, particularly in LIHC, warrants further investigation. These findings highlight SLC16A4 as a promising target for future cancer research and therapy.

Transcriptomic analysis demonstrated that SLC16A3 overexpression selectively downregulates cytokine signalling (reducing CCL5, CCL9, CXCL10) while upregulating CCL8, revealing how this protein contributes to immunosuppression. These findings broaden our understanding of SLC16A3 protein's role in HCC prognosis and sorafenib resistance, indicating that combining SLC16A3 inhibition with sorafenib represents a promising therapeutic strategy.

In germ-free mice, maternal-associated gut Bifidobacterium breve UCC2003 regulates placental endocrine capacity, by altering its metabolic profile and ability to produce endocrine factors. This study provides the first clear evidence that the maternal gut microbiota not only influences placental transport function, but also regulates its endocrine outputs.

Additionally, nodakenetin treatment suppressed the growth of breast cancer cells in nude mice. Our findings suggest that nodakenetin inhibits the viability, promotes apoptosis, and represses glycolysis in breast cancer cells through decreasing SLC16A3 expression, proving the anti-cancer potential of nodakenetin in breast cancer.

Based on multi-omics data from the TCGA database, we further discovered that the low expression of SLC16A4 in lung cancer may be regulated by DNA copy number variations and DNA methylation. In conclusion, this study not only established an efficient diagnostic model for lung cancer but also identified SLC16A4 as a promising biomarker with potential applications in early diagnosis and immunotherapy.

LDHA and SLC16A1 have potential prognostic and diagnostic values for LGG. Therefore, SLC16A1 may serve as a potential biomarker for the diagnosis and treatment of LGG.

SLC16A7 exhibits tumor-suppressive properties, with downregulation in most cancers, and is associated with favorable prognosis and enhanced immune responses. SLC16A7 functions as a tumor suppressor in BCa and is associated with improved survival outcomes. These findings suggest that SLC16A7 is a potential biomarker for cancer diagnosis and prognosis.

Immunohistochemical analyses showed increased PYGL and MCT4 expression correlated with advanced tumor stage, alongside decreased expression of CXCL9 and CXCL10. These findings highlight the critical role of lactate metabolism in HNSCC progression and immunotherapy resistance, identifying PYGL and MCT4 as promising therapeutic targets.