HIF-1α signaling : Essential roles in tumorigenesis and implications in targeted therapies
© 2023 The Authors. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd..
The hypoxic microenvironment is an essential characteristic of most malignant tumors. Notably, hypoxia-inducible factor-1 alpha (HIF-1α) is a key regulatory factor of cellular adaptation to hypoxia, and many critical pathways are correlated with the biological activity of organisms via HIF-1α. In the intra-tumoral hypoxic environment, HIF-1α is highly expressed and contributes to the malignant progression of tumors, which in turn results in a poor prognosis in patients. Recently, it has been indicated that HIF-1α involves in various critical processes of life events and tumor development via regulating the expression of HIF-1α target genes, such as cell proliferation and apoptosis, angiogenesis, glucose metabolism, immune response, therapeutic resistance, etc. Apart from solid tumors, accumulating evidence has revealed that HIF-1α is also closely associated with the development and progression of hematological malignancies, such as leukemia, lymphoma, and multiple myeloma. Targeted inhibition of HIF-1α can facilitate an increased sensitivity of patients with malignancies to relevant therapeutic agents. In the review, we elaborated on the basic structure and biological functions of HIF-1α and summarized their current role in various malignancies. It is expected that they will have future potential for targeted therapy.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 2023 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:11 |
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| Enthalten in: |
Genes & diseases - 11(2023), 1 vom: 18. Jan., Seite 234-251 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Zhao, Yan [VerfasserIn] |
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| Links: |
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| Themen: |
Angiogenesis |
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| Anmerkungen: |
Date Revised 18.08.2023 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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| doi: |
10.1016/j.gendis.2023.02.039 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM360874053 |
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| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a © 2023 The Authors. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. | ||
| 520 | |a The hypoxic microenvironment is an essential characteristic of most malignant tumors. Notably, hypoxia-inducible factor-1 alpha (HIF-1α) is a key regulatory factor of cellular adaptation to hypoxia, and many critical pathways are correlated with the biological activity of organisms via HIF-1α. In the intra-tumoral hypoxic environment, HIF-1α is highly expressed and contributes to the malignant progression of tumors, which in turn results in a poor prognosis in patients. Recently, it has been indicated that HIF-1α involves in various critical processes of life events and tumor development via regulating the expression of HIF-1α target genes, such as cell proliferation and apoptosis, angiogenesis, glucose metabolism, immune response, therapeutic resistance, etc. Apart from solid tumors, accumulating evidence has revealed that HIF-1α is also closely associated with the development and progression of hematological malignancies, such as leukemia, lymphoma, and multiple myeloma. Targeted inhibition of HIF-1α can facilitate an increased sensitivity of patients with malignancies to relevant therapeutic agents. In the review, we elaborated on the basic structure and biological functions of HIF-1α and summarized their current role in various malignancies. It is expected that they will have future potential for targeted therapy | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Review | |
| 650 | 4 | |a Angiogenesis | |
| 650 | 4 | |a Hematological malignancies | |
| 650 | 4 | |a Hypoxia-inducible factor-1 alpha (HIF-1α) | |
| 650 | 4 | |a Immune escape | |
| 650 | 4 | |a Targeted therapy | |
| 700 | 1 | |a Xing, Cheng |e verfasserin |4 aut | |
| 700 | 1 | |a Deng, Yating |e verfasserin |4 aut | |
| 700 | 1 | |a Ye, Can |e verfasserin |4 aut | |
| 700 | 1 | |a Peng, Hongling |e verfasserin |4 aut | |
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