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Updated: Aug 7, 2026
05:58
Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells
Published on: February 24, 2026
Histone Lactylation Mediated by circRNA-Facilitated FXR1 Phase Separation Promotes Colorectal Cancer Progression
Tao Jiang1, Jianquan Liu2, Qihang Hu2
1Affiliated Hospital of Xuzhou Medical College Xuzhou, Jiangsu China.
Cancer Research
|August 5, 2026
Summary
Circular RNA circ2891 drives colorectal cancer (CRC) by boosting glycolysis and histone lactylation. Targeting circ2891 and histone lactylation suppressed tumor growth, offering a new therapeutic strategy for CRC patients.
Area of Science:
- Epigenetics
- Cancer Biology
- Metabolic Reprogramming
Background:
- Histone lactylation, an epigenetic mark from glycolysis, promotes cancer progression by linking metabolism and epigenetics.
- Colorectal cancer (CRC) exhibits metabolic reprogramming crucial for tumor development.
Purpose of the Study:
- To investigate the role of circ2891 in colorectal cancer (CRC) progression.
- To elucidate the mechanism by which circ2891 influences metabolic reprogramming and histone lactylation in CRC.
Main Methods:
- Identified circ2891 in CRC patient tumors.
- Investigated circ2891's interaction with FXR1 and its effect on PGK1 and ENO1 mRNA stability.
- Assessed the impact of circ2891 on aerobic glycolysis, histone lactylation, and DDX21 expression.
- Evaluated therapeutic strategies targeting circ2891 and histone lactylation in preclinical models.
Main Results:
- circ2891 was upregulated in CRC tumors and associated with poor patient outcomes.
- circ2891 enhanced aerobic glycolysis and lactate production, promoting CRC cell proliferation and tumor growth.
- circ2891 stabilized PGK1 and ENO1 mRNAs by facilitating FXR1 phase separation, increasing glycolysis and histone lactylation.
- Elevated glycolysis and histone lactylation activated DDX21, driving CRC progression.
- Combined targeting of circ2891 and histone lactylation inhibited tumor growth in patient-derived organoids and xenografts.
Conclusions:
- circ2891 promotes CRC by stabilizing PGK1/ENO1 via FXR1 phase separation, enhancing glycolysis and histone lactylation to activate DDX21.
- Targeting circ2891 presents a potential therapeutic strategy for improving clinical outcomes in colorectal cancer.
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