Requirement of hypoxia-inducible factor 1 alpha for interleukin 1 beta induced glycolysis in colorectal cancer cells

Verdict. Interleukin-1 beta (IL-1β) is a pro-inflammatory cytokine that is elevated in colorectal cancer. It intersects mitochondrial stress/dysfunction themes (cancer; systemic metabolic stress).

What the authors report

Colorectal cancer cells increase glycolysis to help meet the metabolic demands required for cell growth. Many factors, both endogenous and exogenous, likely drive cellular metabolism and enhance glycolytic flux in colorectal cells.

Key results stated in the abstract include the following. Interleukin-1 beta (IL-1β) is a pro-inflammatory cytokine that is elevated in colorectal cancer. In this study, we investigated the effect of IL-1β toward driving the cancer cell to increase glycolysis, while also suppressing the oxidation of the fiber-derived nutrient butyrate. The results presented here demonstrate that IL-1β stimulated glycolysis and inhibited maximal mitochondrial respiration.

Why it matters for mitochondrial biology

Within mitochondrial research, this work maps primarily to redox biology, metabolism, immunology, cancer. It is relevant to mitochondrial dysfunction discourse because the abstract invokes cancer, systemic metabolic stress. That does not by itself establish a validated disease mechanism; it indicates thematic proximity. Because a therapeutic or interventional angle is present, the piece is of interest for mitochondrial-targeted drug hypothesis generation—subject to full-text validation of endpoints and safety context. Server: biorxiv. Posted 2026-08-16. Synthesis confidence is bounded by abstract completeness.

Study design (abstract-level)

Utilizing colorectal cancer cells with AKT1/2 or HIF1α knocked out showed the requirement of these proteins in mediating the increase in glycolysis following IL-1β treatment.

Principal findings

1. Interleukin-1 beta (IL-1β) is a pro-inflammatory cytokine that is elevated in colorectal cancer.
2. In this study, we investigated the effect of IL-1β toward driving the cancer cell to increase glycolysis, while also suppressing the oxidation of the fiber-derived nutrient butyrate.
3. The results presented here demonstrate that IL-1β stimulated glycolysis and inhibited maximal mitochondrial respiration.
4. IL-1β also increased the phosphorylation of AKT and hypoxia-inducible factor 1 alpha (HIF1α) levels.
5. Our data point to a common pathway through AKT activation and HIF1α upregulation, by which pro-inflammatory cytokines increase glycolysis in colorectal cancer cells to help promote cancer progression.

Limitations of this brief

• This Mitos brief is an abstract-level synthesis of a preprint; it is not peer review and not a substitute for reading the full paper.
• Preprint status: findings may change with revision or journal review.
• Effect sizes, n numbers, statistics, and full experimental controls are typically incomplete at abstract resolution.
• Comparator/control language is weak or absent in the abstract, limiting causal inference from this brief alone.
• Primary source: biorxiv DOI 10.64898/2026.08.11.744327 (posted 2026-08-16).

Open scientific questions

• Which specific experimental panels in the full paper establish the strongest causal claim, and how robust are the controls?
• Are OXPHOS defects primary drivers or secondary consequences of broader cellular stress?
• What dose, timing, and off-target profile would be required to take the intervention seriously as a therapeutic hypothesis?
• How do these findings sit relative to prior literature on the same pathway—replication, contradiction, or incremental extension?

Bottom line

For mitochondrial biologists focused on redox biology, metabolism, immunology, this preprint is worth full-text review if the topic matches your program. Abstract-level takeaway: Interleukin-1 beta (IL-1β) is a pro-inflammatory cytokine that is elevated in colorectal cancer. Confirm methods, effect sizes, and controls in the full PDF before citing the result as established.

Bibliographic record

Abstract-based editorial synthesis by Mitos. Not peer review.