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缺氧诱导因子-1α在多药耐药乳腺癌中的作用

The role of hypoxia-inducible factor-1 alpha in multidrug-resistant breast cancer.

作者信息

Yong Liyun, Tang Shasha, Yu Haixin, Zhang Hongyi, Zhang Yi, Wan Yuan, Cai Fengfeng

机构信息

Department of Breast Surgery, Yangpu Hospital, School of Medicine, Tongji University, Shanghai, China.

Department of Orthopedic Surgery, Yangpu Hospital, School of Medicine, Tongji University, Shanghai, China.

出版信息

Front Oncol. 2022 Aug 8;12:964934. doi: 10.3389/fonc.2022.964934. eCollection 2022.

DOI:10.3389/fonc.2022.964934
PMID:36003773
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9393754/
Abstract

Breast cancer is the most common cancer in women worldwide with increasing incidence. Significant therapeutics advances in the field of breast cancer have resulted in a growing number of treatment options, whereas or acquired resistance is still a persistent clinical challenge. Drug resistance involves a variety of mechanisms, and hypoxia is one of the many causes. Hypoxia-inducible Factor-1 Alpha (HIF-1α) is a key transcription factor which can regulate the response of cells to hypoxia. HIF-1α can trigger anaerobic glycolysis of tumor cells, induce angiogenesis, promote the proliferation, invasion, and migration of tumor cells, and lead to multidrug resistance. This review mainly discusses the role of HIF-1α in the drug-resistant breast cancer and highlighted the potential of HIF-1α -targeted therapy.

摘要

乳腺癌是全球女性中最常见的癌症,其发病率呈上升趋势。乳腺癌领域显著的治疗进展带来了越来越多的治疗选择,然而原发性或获得性耐药仍是一个持续存在的临床挑战。耐药涉及多种机制,缺氧是其中诸多原因之一。缺氧诱导因子-1α(HIF-1α)是一种关键转录因子,可调节细胞对缺氧的反应。HIF-1α可触发肿瘤细胞的无氧糖酵解,诱导血管生成,促进肿瘤细胞的增殖、侵袭和迁移,并导致多药耐药。本综述主要讨论HIF-1α在耐药性乳腺癌中的作用,并强调了以HIF-1α为靶点的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/38bb2babfd60/fonc-12-964934-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/eb612defedb4/fonc-12-964934-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/cfaaa29a2b5f/fonc-12-964934-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/ceae3d08c6e6/fonc-12-964934-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/38bb2babfd60/fonc-12-964934-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/eb612defedb4/fonc-12-964934-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/cfaaa29a2b5f/fonc-12-964934-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/ceae3d08c6e6/fonc-12-964934-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7174/9393754/38bb2babfd60/fonc-12-964934-g004.jpg

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Revisiting the HIF switch in the tumor and its immune microenvironment.
Exploring the interplay between LDHA and ABCC1 in breast cancer using computational approach.
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