Related Experiment Video
Updated: May 28, 2026
05:58
Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells
Published on: February 24, 2026
HNRNPU K181 Lactylation Drives Cervical Cancer Growth by Upregulating PHGDH and Reprogramming Serine Metabolism
Chang Zhang1, Qingfei Meng2, Hui Jiao1
1Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun, China.
Summary
Lactate accumulation in cervical cancer is linked to serine metabolism via HNRNPU lactylation. This post-translational modification promotes tumor growth, offering a potential therapeutic target.
Area of Science:
- Oncology
- Biochemistry
- Molecular Biology
Background:
- Cervical cancer presents a significant global health challenge.
- The molecular drivers of metabolic reprogramming in cervical cancer are not fully understood.
Purpose of the Study:
- To identify novel molecular mechanisms linking lactate accumulation to serine metabolism in cervical cancer.
- To investigate the role of heterogeneous nuclear ribonucleoprotein U (HNRNPU) in cervical cancer progression.
Main Methods:
- Identification of HNRNPU as a lysine lactylation substrate.
- Analysis of HNRNPU binding to PHGDH mRNA.
- In vitro and in vivo studies of cervical cancer cell proliferation.
- Investigation of the interplay between lactylation and acetylation at K181.
- Pharmacological inhibition of HNRNPU lactylation using Pazopanib.
Main Results:
- Lactylation at lysine 181 (K181) stabilizes HNRNPU and enhances its binding to PHGDH mRNA.
- This stabilizes the PHGDH transcript, activating the serine biosynthesis pathway.
- Metabolic reprogramming supports redox homeostasis, nucleotide synthesis, and cancer cell proliferation.
- A competitive interplay between lactylation and acetylation at K181 regulates HNRNPU function.
- Pazopanib inhibits HNRNPU K181 lactylation, suppressing PHGDH expression and tumor growth.
Conclusions:
- HNRNPU K181 lactylation acts as a crucial link between lactate accumulation and serine metabolism in cervical cancer.
- This regulatory axis promotes cancer progression by integrating metabolic signals with post-transcriptional control.
- Targeting HNRNPU lactylation represents a promising therapeutic strategy for cervical cancer.
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