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蛋白质萨尔瓦多同源物1作为一种肿瘤抑制因子,在胰腺导管腺癌中受到高甲基化的调控。

Protein salvador homolog 1 acts as a tumor suppressor and is modulated by hypermethylation in pancreatic ductal adenocarcinoma.

作者信息

Wang Lei, Wang Mei, Hu Chenxi, Li Pengping, Qiao Yun, Xia Youyou, Liu Liang, Jiang Xiaodong

机构信息

Department of Radiation Oncology, Lianyungang First People's Hospital, Jiangsu, People's Republic of China.

Tumor Laboratory, Department of Radiation Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Jiangsu, People's Republic of China.

出版信息

Oncotarget. 2017 May 18;8(38):62953-62961. doi: 10.18632/oncotarget.17972. eCollection 2017 Sep 8.

DOI:10.18632/oncotarget.17972
PMID:28968962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5609894/
Abstract

Salvador (SAV) is a gene product that contains two protein-protein interaction modules known as WW domains and is believed to act as a scaffolding protein for Hippo and Warts. SAV1 is the human homolog of Salvador, which is the most well characterized upstream signaling component of Hippo pathway. Although its role in some tumors is known, SAV1 function in other types of tumors, including pancreatic tumor, is still obscure. Here, we determined the role of SAV1 in pancreatic ductal adenocarcinoma (PDAC) development and progression. Our results revealed that SAV1 suppressed expression promoted PDAC invasion and migration, and repressed pancreatic cancer cells apoptosis. Moreover, SAV1 was silenced by hypermethylation. Thus, SAV1 worked as a cancer suppressor and it might be considered as a target for pancreatic cancer therapy.

摘要

萨尔瓦多(SAV)是一种基因产物,它包含两个被称为WW结构域的蛋白质-蛋白质相互作用模块,并且被认为作为Hippo和Warts的支架蛋白发挥作用。SAV1是萨尔瓦多的人类同源物,它是Hippo通路中特征最明确的上游信号成分。尽管其在某些肿瘤中的作用已为人所知,但SAV1在包括胰腺肿瘤在内的其他类型肿瘤中的功能仍不清楚。在这里,我们确定了SAV1在胰腺导管腺癌(PDAC)发生和发展中的作用。我们的结果显示,SAV1表达抑制促进了PDAC的侵袭和迁移,并抑制了胰腺癌细胞的凋亡。此外,SAV1因高甲基化而沉默。因此,SAV1作为一种抑癌基因发挥作用,它可能被视为胰腺癌治疗的一个靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/0d0475196825/oncotarget-08-62953-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/331a6a784533/oncotarget-08-62953-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/201310eab5a5/oncotarget-08-62953-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/e4e9fbf8c844/oncotarget-08-62953-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/0d0475196825/oncotarget-08-62953-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/331a6a784533/oncotarget-08-62953-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/201310eab5a5/oncotarget-08-62953-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/e4e9fbf8c844/oncotarget-08-62953-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46a7/5609894/0d0475196825/oncotarget-08-62953-g004.jpg

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