Novel insights into SLC16A8 in colorectal cancer

Abstract

Colorectal cancer (CRC) ranks as the third most prevalent cancer globally, and hypoxia-induced metabolic reprogramming is considered a key driver of its malignant progression. We read with interest the article by Tian et al, which examines the role of solute carrier family 16 member 8 (SLC16A8) in regulating the tumor microenvironment. The study provides valuable evidence supporting the dual mechanisms by which SLC16A8 influences CRC pathogenesis and offers new directions for clinical research. This work demonstrates that activation of the HIF-1α/SLC16A8 axis under hypoxic conditions enhances glycolytic flux and lactate production. Additionally, SLC16A8 facilitates lactate transport, thereby inducing endothelial-mesenchymal transition—a finding that underscores its functional significance in shaping the tumor microenvironment. 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.

Keywords: Solute carrier family 16 member 8; Colorectal cancer; Hypoxic; Glycolysis; Tumor microenvironment; Endothelium-mesenchymal transition; siRNA; Genes; Biomarker; Cancer

Core Tip: Solute carrier family 16 member 8 (SLC16A8) drives the progression of the hypoxic microenvironment in colorectal cancer through dual mechanisms: Glycolytic reprogramming mediated by HIF-1α and endothelium-mesenchymal transition. Targeting SLC16A8 synergistically inhibits metabolic adaptation and vascular remodeling, demonstrating potential for clinical translation.