RHOA-dependent regulation of mitochondrial remodeling and cell motility in hypoxia-exposed gastric epithelial cells.

Mitochondrial appearance distinctively reflects cellular stress. Hypoxia, one of the most fundamental stressors, drives tumor progression, impacting mitochondrial structure and function. RAS homolog family member A (RHOA), a key regulator of cell motility, is frequently upregulated in response to hypoxia across cancers.

The influence of hypoxia-mediated CEACAM6 upregulation on epithelial cell and macrophage response in the context of gastric cancer.

Background: The hypoxic microenvironment is a key component of the gastric tumour niche. Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is upregulated in gastric cancer and is considered a novel biomarker for the disease. However, no prior studies have elaborated on the status of CEACAM6 and its role in the hypoxic gastric cancer niche.

Hypoxia-driven metabolic heterogeneity and immune evasive behaviour of gastrointestinal cancers: Elements of a recipe for disaster.

Gastrointestinal (GI) cancers refer to a group of malignancies associated with the GI tract (GIT). Like other solid tumors, hypoxic regions consistently feature inside the GI tumor microenvironment (TME) and contribute towards metabolic reprogramming of tumor-resident cells by modulating hypoxia-induced factors. We highlight here how the metabolic crosstalk between cancer cells and immune cells generate immunosuppressive environment inside hypoxic tumors.