Effect of histone deacetylase 8 gene deletion on breast cancer cellular mechanism in vitro and in vivo study

Rahmani, Golebagh; Moloudi, Mohammad Raman; Amini, Razieh; Rahimi, Karim; Fathi, Fardin; Abdi, Mohammad; Najafi, Rezvan

doi:10.1016/j.lfs.2022.121156

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Small Molecule Drugs Targeting Tnbc1

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2024

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“…HDAC8 can activate YY1 or Hippo/YAP signaling to promote the proliferation and migration of TNBC [ 227 , 228 ]. Down-regulation of HDAC8 can reduce the migration and invasion of TNBC and induce apoptosis in cancer cells [229] . Differently, the expression of HDAC7 is decreased in TNBC patients.…”

Section: Small Molecule Drugs Targeting Tnbcmentioning

confidence: 99%

Small molecule agents for triple negative breast cancer: Current status and future prospects

Ou,

Wang,

et al. 2024

Translational Oncology

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Section: Small Molecule Drugs Targeting Tnbcmentioning

confidence: 99%

Small molecule agents for triple negative breast cancer: Current status and future prospects

Ou,

Wang,

et al. 2024

Translational Oncology

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Exploring the interplay between triple‐negative breast cancer stem cells and tumor microenvironment for effective therapeutic strategies

Zou,

Luo,

Wang

et al. 2024

Journal Cellular Physiology

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Triple‐negative breast cancer (TNBC) is a highly aggressive and metastatic malignancy with poor treatment outcomes. The interaction between the tumor microenvironment (TME) and breast cancer stem cells (BCSCs) plays an important role in the development of TNBC. Owing to their ability of self‐renewal and multidirectional differentiation, BCSCs maintain tumor growth, drive metastatic colonization, and facilitate the development of drug resistance. TME is the main factor regulating the phenotype and metastasis of BCSCs. Immune cells, cancer‐related fibroblasts (CAFs), cytokines, mesenchymal cells, endothelial cells, and extracellular matrix within the TME form a complex communication network, exert highly selective pressure on the tumor, and provide a conducive environment for the formation of BCSC niches. Tumor growth and metastasis can be controlled by targeting the TME to eliminate BCSC niches or targeting BCSCs to modify the TME. These approaches may improve the treatment outcomes and possess great application potential in clinical settings. In this review, we summarized the relationship between BCSCs and the progression and drug resistance of TNBC, especially focusing on the interaction between BCSCs and TME. In addition, we discussed therapeutic strategies that target the TME to inhibit or eliminate BCSCs, providing valuable insights into the clinical treatment of TNBC.

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Effect of histone deacetylase 8 gene deletion on breast cancer cellular mechanism in vitro and in vivo study

Cited by 2 publications

References 30 publications

Small molecule agents for triple negative breast cancer: Current status and future prospects

Small molecule agents for triple negative breast cancer: Current status and future prospects

Exploring the interplay between triple‐negative breast cancer stem cells and tumor microenvironment for effective therapeutic strategies

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