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中国生物工程杂志

China Biotechnology
China Biotechnology
China Biotechnology  2023, Vol. 43 Issue (2/3): 104-119    DOI: 10.13523/j.cb.2209072
    
Functional Studies of AMOT Family Members and Their Potential Applications in Cancer Therapy
ZHANG Xin1,2,3,4,ZHANG Rui1,2,3,4,**(),TANG Jing-feng1,2,3,4,**()
1 National “111” Center for Cellular Regulation and Molecular Pharmaceutics, Hubei University of Technology, Wuhan 430068, China
2 Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei University of Technology, Wuhan 430068, China
3 Cooperative Innovation Center of Industrial Fermentation (Ministry of Education & Hubei Province), Hubei University of Technology, Wuhan 430068, China
4 Hubei Key Laboratory of Industrial Microbiology, Hubei University of Technology, Wuhan 430068, China
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Abstract  

Angiomotin(AMOT) is a type of angiogenesis inhibitor binding protein. Members of the AMOT family (AMOTs) are involved in various critical biological processes, for example, cell proliferation, cell migration, angiogenesis, and virus release. AMOTs expressed in most cancer and regulate cancer development and progression. Available evidence suggests that AMOTs act as both tumor promoters and tumor suppressors, and this opposite regulation in cancer still needs to be validated. This review focuses on the structure, expression localization, and function of AMOTs, and additionally, it systematically summarizes previous research and therapeutic roles in cancer. It discusses the possibility and challenges of treating cancer through AMOTs.

Key words： Angiomotin family      Biological functions      Cancer      Therapeutic target     
Received: 27 September 2022      Published: 31 March 2023
ZTFLH:  Q819  
Corresponding Authors: **Rui ZHANG,Jing-feng TANG     E-mail: zhangrui1987@hbut.edu.cn;tangjingfeng@hbut.edu.com
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Xin ZHANG
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Cite this article:

ZHANG Xin, ZHANG Rui, TANG Jing-feng. Functional Studies of AMOT Family Members and Their Potential Applications in Cancer Therapy. China Biotechnology, 2023, 43(2/3): 104-119.

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https://manu60.magtech.com.cn/biotech/10.13523/j.cb.2209072     OR     https://manu60.magtech.com.cn/biotech/Y2023/V43/I2/3/104

Fig.1 Schematic diagram of the domains of each member of the AMOT protein family
Fig.2 mRNA expression levels of each member of the AMOT protein family in different human tissues (The results are from The Human Protein Atlas database)
AMOT家族 相互作用蛋白 结构域或基序 可能的功能 参考文献
AMOT YAP1/TAZ/AIP4 L/PPxY基序 调节细胞增殖和癌症发展 [40,54]
14-3-3 RSLSERLMQ 胞质滞留 [55]
LATS1/2 HVRSLS 磷酸化、刺激LATS激酶自磷酸化 [34,52]
Merlin/RICK Colied-coil结构域 调节细胞迁移和细胞连接 [54]
Patj PDZ 结合基序 调节细胞迁移和细胞连接 [54]
RICH1 Colied-coil结构域 激活Hippo信号 [17]
WWOX L/PPxY基序 调节丝状病毒VP40 VLPs的排出 [56]
F-actin F-actin结合基序 调节YAP定位 [19]
KIF13B 未知 调节纤毛长度、成分和信号 [57]
NEDD4L L/PPxY基序 刺激HIV-1包膜并促进传染性 [18]
eIF4A 238~255氨基酸 限制球蛋白质合成 [58]
UCA1 Colied-coil结构域 促进YAP去磷酸化和核易位 [6]
RNF146/TNKS N-terminal结构域 调节β-catenin的稳定性;维持细胞连接处
的Crumbs复合体		 [49,59]
PAR6 PDZ 结合基序 通过细胞极性变化促进细胞迁移 [2]
BMPR2/SMAD1 未知 调节BMP靶基因表达 [60]
MUPP1/PSD-95 未知 控制肌动蛋白周转和PSD完整性 [61]
Rho Colied-coil结构域 调节AMOT的分布和磷酸化 [62]
AMOT家族 相互作用蛋白 结构域或基序 可能的功能 参考文献
TFPI-1 未知 激活Hippo信号 [63]
PKCι Colied-coil结构域 磷酸化和调节核YAP定位 [36]
USP9X Colied-coil结构域 脱乙酰基化 [40]
Par/Crb PDZ结合基序 内分泌循环 [64]
sCD146 未知 促进血管生成 [65]
Cad11 Middle domain 细胞迁移 [53]
NEDD4/ITCH L/PPxY基序 泛素化 [41]
CDH1 未知 激活LATS1/2 [66]
AMOTL1 LATS1/2 HVRSLS 磷酸化 [34]
YAP1 L/PPxY基序 增加YAP稳定性 [67]
PIV5 M C-terminal结构域 调节副黏病毒出芽 [46]
NEDD4L/ NEDD4/ HECW1 L/PPxY基序 泛素化;招募副黏病毒M蛋白 [46]
USP9X Colied-coil结构域 去泛素化 [40]
RNF146/TNKS N-terminal结构域 维持细胞连接处的Crumbs复合体 [49]
N-cadherin 未知 影响血管生成 [68]
Fat4 未知 介导Fat4信号转导 [30]
AMPK Ser793 磷酸化 [37]
HECW2 L/PPxY基序 泛素化 [44]
AMOTL2 LATS1/2 HVRSLS 磷酸化 [34]
Par3 未知 调节细胞连接定位 [69]
USP9X Colied-coil结构域 去泛素化 [40]
RNF146/TNKS N-terminal结构域 维持细胞连接处的Crumbs复合体 [49]
β-catenin Colied-coil/ N-terminal 结构域 抑制Wnt/β-catenin信号 [70]
mTORC2 402~512 氨基酸 磷酸化 [38]
c-Src 未知 调节易位 [71]
WWP1 L/PPxY基序 泛素化 [42]
PPP2R2A 1~103 氨基酸 抑制JUN Thr239去磷酸化 [72]
LL5β 未知 未知 [73]
AKT 未知 抑制AKT信号 [74]
Table 1 Interacting proteins, binding domains, and corresponding functions of AMOTs
癌症类型 异构体 功能 可能分子机制 参考文献
乳腺癌 AMOT-P80 致癌基因 抑制Hippo信号 [17]
AMOT-P130 抑癌基因 抑制Wnt/β-catenin信号;调节Rho通路;抑制YAP的激活 [10,34,59]
AMOT 致癌基因 激活YAP-ERK信号通路 [115]
AMOTL1 致癌基因 激活Src [116]
AMOTL2 致癌基因 破坏顶端-基底细胞极性 [111]
弥漫性大B细胞淋巴瘤 AMOT-P130 抑癌基因 调节DNA损伤反应信号 [11]
胃癌 AMOTL1 致癌基因 增强YAP稳定性 [67]
AMOT-P130 抑癌基因 抑制上皮间质转化 [9]
肺癌 AMOT-P130 抑癌基因 抑制与SMAD2/3信号通路无关的血管生成拟态形成 [117]
AMOT 抑癌基因 稳定AMOT并抑制YAP信号;阻断致癌基因YAP/TAZ
并降低Cyr61表达		 [48,118]
AMOTL2 抑癌基因 通过结合PPP2R2A抑制JUN Thr239去磷酸化 [72]
骨肉瘤 AMOT 致癌基因 未知 [112]
肝癌 AMOT-P130 致癌基因 促进YAP激活 [12]
AMOTL2 致癌基因 未知 [119]
卵巢癌 AMOT-P130 抑癌基因 抑制YAP靶基因的激活 [36]
AMOT-P130 致癌基因 促进YAP去磷酸化和核易位 [6]
前列腺癌 AMOT-P80 致癌基因 调节Cad11介导的细胞迁移;抑制Hippo信号 [53,106]
头颈部鳞状细胞癌 AMOT-P80 致癌基因 未知 [113]
肾细胞癌 AMOT 致癌基因 增加YAP相关的TEAD启动子活性 [29]
宫颈癌 AMOTL1 致癌基因 未知 [28,114]
结肠癌 AMOT 致癌基因 激活YAP-ERK/PI3K-AKT信号通路 [101]
AMOTL2 致癌基因 破坏顶端-基底细胞极性 [28]
胶质母细胞瘤 AMOTL1 致癌基因 增强YAP信号的激活 [7]
AMOTL2 抑癌基因 抑制YAP靶基因激活;调控β-catenin核定位 [38,87]
血管内皮瘤 AMOT-P80 致癌基因 促进血管生成 [113]
鼻窦内翻性乳头状瘤 AMOT 致癌基因 未知 [113]
胰腺癌 AMOTL2 致癌基因 促进血管生成 [8]
Table 2 The roles and possible regulatory mechanisms of AMOTs in different cancers
Fig.3 Schematic diagram of molecular mechanisms related to AMOT
Fig.4 Schematic diagram of molecular mechanisms related to AMOTL1 and AMOTL2
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