Gastroenterology：mTORC1/2聚集在Arp2/3复合体上促进腺泡→导管化生→早期胰腺癌转化进展

2021-01-05 MedSci原创 MedSci原创

致癌基因Kras通过以肌动蛋白为基础的形态发生过程-腺泡-导管化生(ADM)诱导胰腺腺泡细胞的肿瘤转化，并导致胰腺导管腺癌(PDAC)。mTOR复合物1(mTORC1)和2(mTORC2)分别含有Rp

致癌基因Kras通过以肌动蛋白为基础的形态发生过程-腺泡-导管化生(ADM)诱导胰腺腺泡细胞的肿瘤转化，并导致胰腺导管腺癌(PDAC)。mTOR复合物1(mTORC1)和2(mTORC2)分别含有Rptor和Rictor，并在Kras下游被激活，从而促进PDAC的形成。然而，mTORC1和mTORC2是否以及如何影响ADM，以及介导这种肌动蛋白重排的肌动蛋白核因子的身份仍不清楚。

采用炎症加速Kras诱导的小鼠早期胰腺癌模型。在腺泡细胞中，条件性消融Rptor、Rictor或Arpc4(肌动蛋白相关蛋白2/3复合体4)以激活mTORC1、mTORC2和肌动蛋白相关蛋白(Arp)2/3复合体的功能。

mTORC1和mTORC2协同促进KrasG12D诱导的ADM和胰腺癌发生

结果发现，mTORC1和mTORC2在人和小鼠的ADM病变中被显著激活，并在小鼠体内和体外协同促进Kras驱动的ADM。它们利用Arp2/3复合体作为共同的下游效应器来诱导肌动蛋白细胞骨架重塑，从而导致ADM。此外，mTORC1调控Rac1(Rac家族小GTPase 1)和Arp2/3-复合体亚基Arp3的翻译，而mTORC2通过促进Akt/Rac1信号通路激活Arp2/3复合体。

mTORC2通过Akt/Rac1信号轴激活Arp2/3复合物

与上述结果一致，消融Arp2/3复合体基因可以在体内阻止Kras驱动的ADM。在腺泡细胞中，Arp2/3复合体及其肌动蛋白核活性介导了基底外侧肌动蛋白皮质的形成，这是ADM和癌前转化所必需的。

本研究表明，mTORC1和mTORC2通过促进Arp2/3复合体功能，在ADM和早期胰腺癌发生中起到双重但非冗余的调节作用。因此，Arp2/3复合体作为mTORC1和mTORC2的共同效应器填补了致癌信号和PDAC启动的肌动蛋白动力学之间的空白。

原始出处：

Zhao Yamin,Schoeps Benjamin,Yao Dianbo et al. mTORC1 and mTORC2 converge on the Arp2/3 complex to promote Kras-induced acinar-to-ductal metaplasia and early pancreatic carcinogenesis.[J] .Gastroenterology, 2020, 10.1053/j.gastro.2020.12.061.

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2021-10-03 jktdtl

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2021-11-05 ms24272190615788285182

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2021-07-08 许安

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2021-06-07 bioon1

#复合体#

78 0
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2021-01-07 雕雕

#mTORC1#

51 0
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2021-01-07 chaojitidian

#Gastroenterology#

66 0
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2021-01-05 Nebula-Qin

#肿瘤#胰腺癌

139 0

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肿瘤科

Gastroenterology：mTORC1/2聚集在Arp2/3复合体上促进腺泡→导管化生→早期胰腺癌转化进展

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