Targeting hypoxia-inducible factor-1alpha: A new strategy for triple-negative breast cancer therapy - 15/11/22
, Chengcheng Guan a, 1 , Cui Liu b , Huayao Li b , Jibiao Wu c , Changgang Sun b, d, ⁎ Abstract |
Triple-negative breast cancer (TNBC) is a subtype of breast cancer that is highly aggressive and hypoxic compared with other subtypes. The role of hypoxia inducible factor 1α (HIF-1α) as a key hypoxic transcription factor in oncogenic processes has been extensively studied. Recently, it has been shown that HIF-1α regulates the complex biological processes of TNBC, such as glycolysis, angiogenesis, invasion and metastasis, breast cancer stem cells (BCSCs) enrichment, and immune escape, to promote TNBC survival and development through the activation of downstream target genes. In addition, inflammatory mediators, oxygen levels, noncoding RNAs, complex signaling regulatory networks, epigenetic regulators are involved in the upstream regulatory expression of HIF-1α. However, further studies are needed to determine the potential and future directions of targeting HIF-1α in TNBC. This article discusses the expression of the HIF-1α transcription factor in TNBC. We also explored the mechanism by which HIF-1α drives TNBC progression. The potential significance of targeting HIF-1α for immunotherapy, chemotherapy, anti-angiogenic therapy, and photodynamic therapy is discussed. The intrinsic mechanism, existing problems and future directions of targeting HIF-1α are also studied.
Le texte complet de cet article est disponible en PDF.Highlights |
• | Compared with other subtypes of breast cancer, triple-negative breast cancer has obvious hypoxia characteristics and rich expression of HIF-1α. |
• | In triple-negative breast cancer, HIF-1α is regulated by the NF-κB, RAS-RAF-MEK-ERK, PI3K/Akt/mTOR, and JAK-STAT signaling pathways. |
• | HIF-1α is regulated by the level of oxygen contained in the tumor. |
• | In triple negative breast cancer, HIF-1α can be targeted by reducing the expression level of HIF-1α, promoting HIF-1α protein degradation, inhibiting HIF-1α protein synthesis and inhibiting HIF-1α dimerization. |
Abbreviations : TNBC, HIF-1α, BCSCs, LDHA, HER-2, PR, ER, PDT, NO, ROS, PHD-2, ODDD, VHL, FIH, HRE, IκKB, IκB, IκBα, COX-2, LOX, GLUT1, PDK1, LDHA, MCTs, VEGF, HGF, VCAM1, C1QBP, EMT, MMP-9, MMP-2, Brk, ITGA5, MEK, GSH, MEK, DUSPs, A2BR, TAMs, DCs, CSF1, CCL5, CCR5, GM-CSF, PFS, MSCs, Tregs, CTLA-4, CXCR4, FoxP3, TAX, ADR, GEM, DHA, EPA, FDA, OS, C15H24, ISL, AHI, MEL, As4S4, IFP, HSP90, PKM2, ZEB1, NANOG, KLF4, MDSCs, HAT, HDAC, TET, 5mC, 5hmC, S1P, SPHK2, DATS
Keywords : HIF-1α, Triple-negative breast cancer, Signaling pathways, Hypoxia, TNBC progression, Combination therapy
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Vol 156
Article 113861- décembre 2022 Retour au numéro
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