Loading
Life sciences · Journal article
Cell Death and Disease · September 28, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Abstract High-fat diet (HFD) is known to promote colorectal cancer (CRC) tumorigenicity. Lactate-induced protein lysine lactylation plays a critical role in the progression of malignancies; however, its significance in HFD-driven cancer remains unclear. Here, using a genetically engineered mouse model, we observe enhanced glycolytic metabolism and elevated levels of lactylation in HFD-driven CRC. By performing a screen of the lactylated proteome, we identify that triosephosphate isomerase (TPI1) undergoes lactylation at lysine residues 142 and 188. This lactylation enhances TPI1’s activity to convert dihydroxyacetone phosphate to glyceraldehyde 3-phosphate via conformational changes, thereby directing phospholipid synthesis toward glycolysis in cancer cells. This metabolic rewiring contributes to HFD-induced CRC tumorigenesis. Moreover, the interaction between TPI1 and aldolase A (ALDOA), which is strengthened by TPI1 lactylation, facilitates glycolysis in HFD-associated CRC. Cell-penetrating peptides designed to competitively inhibit TPI1 lactylation effectively suppress HFD-related CRC progression. Clinically, TPI1 lactylation correlates with poor prognosis in obese patients with CRC. Thus, TPI1 lactylation serves as a key signal coordinating lipid and glucose metabolism, and may represent a therapeutic target for HFD-driven cancer.