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浙江大学学报（医学版）
浙江大学学报（医学版）  2022, Vol. 51 Issue (2): 241-250    DOI: 10.3724/zdxbyxb-2021-0297
综述     
恶性肿瘤饥饿疗法研究现状
李健宜,佟丹丹,林俊生()
华侨大学医学院，福建 泉州 362021
Current status of cancer starvation therapy
LI Jianyi,TONG Dandan,LIN Junsheng()
School of Medicine, Huaqiao University, Quanzhou 362021, Fujian Province, China
 全文: PDF(4419 KB)   HTML( 34 )
摘要：

恶性肿瘤传统的治疗方法各有局限和弊端。近年来新兴的饥饿疗法通过阻断肿瘤的营养供应，达到“饿死”肿瘤细胞的目的。饥饿疗法的治疗策略主要包括：通过靶向抑制促血管生成因子及其受体和整合素，干预肿瘤血管生成机制，以抗肿瘤血管生成；通过栓塞和挤压血管，以阻断肿瘤血管的输血供氧功能；通过抑制线粒体的丝氨酸/甘氨酸/一碳代谢、抑制糖酵解、抑制氨基酸代谢等方式抑制肿瘤细胞代谢过程；饥饿疗法与氧化疗法、化学治疗、声动力疗法、抑制肿瘤细胞自噬等方法联合可以达到协同效果。本文从以上四个方面总结近年来肿瘤饥饿疗法的研究进展和存在的问题，以期对恶性肿瘤治疗策略的选择有所帮助。
关键词： 肿瘤;  饥饿疗法;  抗血管生成;  肿瘤代谢;  协同治疗;  综述    
Abstract:

Conventional therapies for malignant tumors have limitations and disadvantages. In recent years, the cancer starvation therapy has emerged which intends to deprive cancer cells of nutritional supply. There are several approaches to“starve” cancer cells: to intervene tumor angiogenesis by targeted inhibition of angiogenic factors or their receptors and integrins; to block the blood supply of cancer cells by embolizing or compressing blood vessels; to intervene metabolic process of cancer cells by inhibition of the signal pathways of mitochondrial serine-glycine-one earbon metabolism, glycolysis and amino acid metabolism; cancer starvation therapy can be employed with oxidation therapy, chemotherapy, sonodynamic therapy, anti-autophagy therapy or other therapies to achieve synergistic effects. This article reviews the research progress of cancer starvation therapy in recent years and discusses the existing problems.
Key words: Neoplasms    Starvation therapy    Anti-angiogenesis    Tumor metabolism    Synergistic therapy    Review
收稿日期: 2021-09-28 出版日期: 2022-08-02
CLC:  R73  
基金资助: 国家重点研发计划（2016YFE0101700）；华侨大学高层次人才引进项目（13Y0391）
通讯作者: 林俊生     E-mail: junshenglin@hqu.edu.cn
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李健宜
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引用本文:

李健宜,佟丹丹,林俊生. 恶性肿瘤饥饿疗法研究现状[J]. 浙江大学学报（医学版）, 2022, 51(2): 241-250.

LI Jianyi,TONG Dandan,LIN Junsheng. Current status of cancer starvation therapy. J Zhejiang Univ (Med Sci), 2022, 51(2): 241-250.

链接本文:

https://www.zjujournals.com/med/CN/10.3724/zdxbyxb-2021-0297    或    https://www.zjujournals.com/med/CN/Y2022/V51/I2/241

图 1  抗肿瘤血管生成机制示意图促血管生成因子和整合素广泛参与血管生成，酪氨酸激酶是参与许多信号通路的关键酶，单克隆抗体（如贝伐珠单抗）可靶向促血管生成因子或其受体；RBM-007适体可靶向成纤维细胞生长因子2；西仑吉肽和自组装肽纳米粒可靶向整合素αvβ3，OS2966抗体可靶向整合素β1；索拉非尼等小分子化合物可靶向酪氨酸激酶，从而实现抗肿瘤血管生成. 血管生成模式从出芽式转换成套叠式可导致肿瘤产生耐药性，上调、、、和基因表达可抑制套叠式血管生成药物从而改善耐药性. CXCL：趋化因子CXC亚家族配体；ACTA：α-肌动蛋白；CALD：钙调蛋白结合蛋白；TEM：肿瘤内皮标志物；COUP-TF：鸡卵清蛋白上游启动子转录因子.
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