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Peer-reviewedCC BY 4.0Communications Biology

Lactate drives the emergence of tumor cells with centrosome amplification through CP110 lactylation

  • Xiaoqian Wu
  • Rui Miao
  • Shuning Ding
  • Yanchun Quan
  • Ting Zhu
  • Fanyi Zhang
  • Deyue Liu
  • Hongwei Chen
  • Hui Cao
  • Yu Zhang
  • Yan Fang
  • Jingxuan Xu
14 more authors
  • Yin Shou
  • Qian Wang
  • Yan Liu
  • Yuming Li
  • Jianhua Chen
  • Lianhui Sun
  • Ying Lin
  • Jun Liu
  • Lei Chen
  • Ting Xu
  • Wei Wang
  • Yanqiang Hou
  • Guangjian Fan
  • Li Zhu
Open at sourceDOICite

Abstract

Centrosome amplification (CA) is a critical driver of tumor heterogeneity and subsequent cancer progression and metastasis. However, the cellular origin of CA has not been fully elucidated, specifically whether CA arises from progenitor cells with pre-existing centrosome abnormalities or develops de novo in initially normal tumor cells. In this study, we demonstrate that lactate, a metabolic feature commonly enriched in tumor tissues, induces the transformation of cells with two centrosomes into cells with CA, thereby providing an explanation for the widespread presence of CA in tumors. Mechanistically, through systematic screening of centrosomal proteins, we identified CP110 and its key lactylation site at lysine 690 (K690), as critical drivers of CA in tumor cells. Furthermore, CP110-K690 lactylation promotes genomic instability, accelerates cellular proliferation, and enhances metastatic potential by driving CA, collectively facilitating malignant progression. Importantly, inhibition of CP110-K690 lactylation effectively disrupts this pro-tumorigenic signaling axis. Collectively, these findings identify CP110-K690 lactylation as an upstream molecular mechanism underlying the pervasive occurrence of CA across diverse tumor types and its role in promoting aggressive tumor behavior.

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Cite

BibTeXRIS
BibTeX
@article{wu2026lactate,
  title = {{Lactate drives the emergence of tumor cells with centrosome amplification through CP110 lactylation}},
  author = {Xiaoqian Wu and Rui Miao and Shuning Ding and Yanchun Quan and Ting Zhu and Fanyi Zhang and Deyue Liu and Hongwei Chen and Hui Cao and Yu Zhang and Yan Fang and Jingxuan Xu and Yin Shou and Qian Wang and Yan Liu and Yuming Li and Jianhua Chen and Lianhui Sun and Ying Lin and Jun Liu and Lei Chen and Ting Xu and Wei Wang and Yanqiang Hou and Guangjian Fan and Li Zhu},
  journal = {Communications Biology},
  year = {2026},
  month = oct,
  doi = {10.1038/s42003-026-10998-z},
  url = {https://www.nature.com/articles/s42003-026-10998-z},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Lactate drives the emergence of tumor cells with centrosome amplification through CP110 lactylation
AU  - Xiaoqian Wu
AU  - Rui Miao
AU  - Shuning Ding
AU  - Yanchun Quan
AU  - Ting Zhu
AU  - Fanyi Zhang
AU  - Deyue Liu
AU  - Hongwei Chen
AU  - Hui Cao
AU  - Yu Zhang
AU  - Yan Fang
AU  - Jingxuan Xu
AU  - Yin Shou
AU  - Qian Wang
AU  - Yan Liu
AU  - Yuming Li
AU  - Jianhua Chen
AU  - Lianhui Sun
AU  - Ying Lin
AU  - Jun Liu
AU  - Lei Chen
AU  - Ting Xu
AU  - Wei Wang
AU  - Yanqiang Hou
AU  - Guangjian Fan
AU  - Li Zhu
PY  - 2026
DA  - 2026/10/27
JO  - Communications Biology
DO  - 10.1038/s42003-026-10998-z
UR  - https://www.nature.com/articles/s42003-026-10998-z
AB  - Centrosome amplification (CA) is a critical driver of tumor heterogeneity and subsequent cancer progression and metastasis. However, the cellular origin of CA has not been fully elucidated, specifically whether CA arises from progenitor cells with pre-existing centrosome abnormalities or develops de novo in initially normal tumor cells. In this study, we demonstrate that lactate, a metabolic feature commonly enriched in tumor tissues, induces the transformation of cells with two centrosomes into cells with CA, thereby providing an explanation for the widespread presence of CA in tumors. Mechanistically, through systematic screening of centrosomal proteins, we identified CP110 and its key lactylation site at lysine 690 (K690), as critical drivers of CA in tumor cells. Furthermore, CP110-K690 lactylation promotes genomic instability, accelerates cellular proliferation, and enhances metastatic potential by driving CA, collectively facilitating malignant progression. Importantly, inhibition of CP110-K690 lactylation effectively disrupts this pro-tumorigenic signaling axis. Collectively, these findings identify CP110-K690 lactylation as an upstream molecular mechanism underlying the pervasive occurrence of CA across diverse tumor types and its role in promoting aggressive tumor behavior.
SN  - 2399-3642
ER  -