Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation

Abstract Triple-negative breast cancer (TNBC) continues to pose a significant obstacle in the field of oncology. Dysregulation of lipid metabolism, notably upregulated ketogenesis, has emerged as a hallmark of TNBC, yet its role in metastasis has been elusive. Here, by utilizing clinical specimens a...

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Main Authors: Haoran Jiang, Yuan Zeng, Xiaoye Yuan, Liwen Chen, Xuni Xu, Xue Jiang, Quan Li, Gang Li, Han Yang
Format: Article
Language:English
Published: BMC 2024-11-01
Series:Lipids in Health and Disease
Subjects:
Online Access:https://doi.org/10.1186/s12944-024-02364-x
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author Haoran Jiang
Yuan Zeng
Xiaoye Yuan
Liwen Chen
Xuni Xu
Xue Jiang
Quan Li
Gang Li
Han Yang
author_facet Haoran Jiang
Yuan Zeng
Xiaoye Yuan
Liwen Chen
Xuni Xu
Xue Jiang
Quan Li
Gang Li
Han Yang
author_sort Haoran Jiang
collection DOAJ
description Abstract Triple-negative breast cancer (TNBC) continues to pose a significant obstacle in the field of oncology. Dysregulation of lipid metabolism, notably upregulated ketogenesis, has emerged as a hallmark of TNBC, yet its role in metastasis has been elusive. Here, by utilizing clinical specimens and experimental models, the study demonstrates that increased ketogenesis fosters TNBC metastasis by promoting the up-regulation of β-hydroxybutyrate (β-OHB), a key ketone body. Mechanistically, β-OHB facilitates β-hydroxybutyrylation (Kbhb) of Calpastatin (CAST), an endogenous calpain (CAPN) inhibitor, at K43, blocking the interaction with CAPN and subsequently promoting FAK phosphorylation and epithelial‒mesenchymal transition (EMT). In conclusion, the study reveals a novel regulatory axis linking ketogenesis to TNBC metastasis, shedding light on the intricate interplay between metabolic reprogramming and tumor progression.
format Article
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institution Kabale University
issn 1476-511X
language English
publishDate 2024-11-01
publisher BMC
record_format Article
series Lipids in Health and Disease
spelling doaj-art-90a580d05b324c719707e22699cc1e0b2024-11-17T12:46:16ZengBMCLipids in Health and Disease1476-511X2024-11-0123111110.1186/s12944-024-02364-xKetogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylationHaoran Jiang0Yuan Zeng1Xiaoye Yuan2Liwen Chen3Xuni Xu4Xue Jiang5Quan Li6Gang Li7Han Yang8Department of Radiation Oncology, The First Affiliated Hospital of Wenzhou Medical UniversityDepartment of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical UniversityDepartment of Radiation Oncology, The First Affiliated Hospital of Wenzhou Medical UniversityDepartment of Radiation Oncology, The First Affiliated Hospital of Wenzhou Medical UniversityDepartment of Radiation Oncology, The First Affiliated Hospital of Wenzhou Medical UniversityDepartment of Radiation Oncology, The First Affiliated Hospital of Wenzhou Medical UniversityDepartment of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical UniversityDepartment of Radiation Oncology, The First Affiliated Hospital of Wenzhou Medical UniversityDepartment of Internal Medicine-Oncology, The First Affiliated Hospital of Wenzhou Medical UniversityAbstract Triple-negative breast cancer (TNBC) continues to pose a significant obstacle in the field of oncology. Dysregulation of lipid metabolism, notably upregulated ketogenesis, has emerged as a hallmark of TNBC, yet its role in metastasis has been elusive. Here, by utilizing clinical specimens and experimental models, the study demonstrates that increased ketogenesis fosters TNBC metastasis by promoting the up-regulation of β-hydroxybutyrate (β-OHB), a key ketone body. Mechanistically, β-OHB facilitates β-hydroxybutyrylation (Kbhb) of Calpastatin (CAST), an endogenous calpain (CAPN) inhibitor, at K43, blocking the interaction with CAPN and subsequently promoting FAK phosphorylation and epithelial‒mesenchymal transition (EMT). In conclusion, the study reveals a novel regulatory axis linking ketogenesis to TNBC metastasis, shedding light on the intricate interplay between metabolic reprogramming and tumor progression.https://doi.org/10.1186/s12944-024-02364-xBreast cancerMetastasisKetogenesisβ-hydroxybutyrylationEpithelial–mesenchymal transition
spellingShingle Haoran Jiang
Yuan Zeng
Xiaoye Yuan
Liwen Chen
Xuni Xu
Xue Jiang
Quan Li
Gang Li
Han Yang
Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation
Lipids in Health and Disease
Breast cancer
Metastasis
Ketogenesis
β-hydroxybutyrylation
Epithelial–mesenchymal transition
title Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation
title_full Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation
title_fullStr Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation
title_full_unstemmed Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation
title_short Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation
title_sort ketogenesis promotes triple negative breast cancer metastasis via calpastatin β hydroxybutyrylation
topic Breast cancer
Metastasis
Ketogenesis
β-hydroxybutyrylation
Epithelial–mesenchymal transition
url https://doi.org/10.1186/s12944-024-02364-x
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