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肝细胞癌中ATP6V1G1调控的磷酸化蛋白的鉴定与验证

Identification and validation of ATP6V1G1-regulated phosphorylated proteins in hepatocellular carcinoma.

作者信息

Zhang Yi, Lu Liuyi, Chen Mingxing, Nie Jiaqi, Qin Xue, Chen Huaping

机构信息

Department of Clinical Laboratory, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education Nanning, The First Affiliated Hospital of Guangxi Medical University, Guangxi, China.

Department of Clinical Laboratory, Guangxi International Zhuang Medicine Hospital, Nanning, Guangxi, China.

出版信息

PLoS One. 2024 Dec 2;19(12):e0310037. doi: 10.1371/journal.pone.0310037. eCollection 2024.

DOI:10.1371/journal.pone.0310037
PMID:39621600
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11611105/
Abstract

V-ATPase Subunit G1 (ATP6V1G1) is one of the subunits of Vacuolar ATPases. Previous studies have indicated that ATP6V1G1 plays important roles in hepatocellular carcinoma (HCC) and is associated with HCC progression. However, the effect of ATP6V1G1 in HCC requires further elucidation. The aim of the present study was to explore the roles of ATP6V1G1 in HCC and further decipher the detailed mechanism. To identify the phosphorylated proteins regulated by ATP6V1G1 in HCC, phosphoproteomics and LC-MS/MS analysis were performed on HepG2 with overexpression of ATP6V1G1 and empty vector. Western blotting was applied to validate the differentially expressed phosphorylated proteins (DEPPs). As a result, 163 DEPPs were identified by proteomics; two up-regulated phosphorylated proteins (p-RPS6(Ser235)) and (p-SQSTM1(Ser272)) and two down-regulated phosphorylated proteins (p-PDPK1(Ser241)) and (p-EEF2 (Ser57)) were validated. Taken together, this study highlighted the potential impact of ATP6V1G1 on tumor progression, which may be beneficial to liver cancer related basic research.

摘要

V-ATP酶亚基G1(ATP6V1G1)是液泡ATP酶的亚基之一。先前的研究表明,ATP6V1G1在肝细胞癌(HCC)中起重要作用,并与HCC进展相关。然而,ATP6V1G1在HCC中的作用仍需进一步阐明。本研究的目的是探讨ATP6V1G1在HCC中的作用,并进一步解析其详细机制。为了鉴定HCC中受ATP6V1G1调控的磷酸化蛋白,对过表达ATP6V1G1和空载体的HepG2细胞进行了磷酸化蛋白质组学和液相色谱-串联质谱分析。采用蛋白质免疫印迹法验证差异表达的磷酸化蛋白(DEPPs)。结果,通过蛋白质组学鉴定出163个DEPPs;验证了两种上调的磷酸化蛋白(p-RPS6(Ser235))和(p-SQSTM1(Ser272))以及两种下调的磷酸化蛋白(p-PDPK1(Ser241))和(p-EEF2 (Ser57))。综上所述,本研究突出了ATP6V1G1对肿瘤进展的潜在影响,这可能有利于肝癌相关的基础研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/9c027c3a3909/pone.0310037.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/599fd9f9fa48/pone.0310037.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/791ff10a964a/pone.0310037.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/c13d375b7ac1/pone.0310037.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/9c027c3a3909/pone.0310037.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/599fd9f9fa48/pone.0310037.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/791ff10a964a/pone.0310037.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/c13d375b7ac1/pone.0310037.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7816/11611105/9c027c3a3909/pone.0310037.g004.jpg

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[Numb activates the mTORC1 signaling pathway in proximal tubular epithelial cells by upregulating V1G1 expression].[麻木通过上调V1G1表达激活近端肾小管上皮细胞中的mTORC1信号通路]
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HuaChanSu suppresses tumor growth and interferes with glucose metabolism in hepatocellular carcinoma cells by restraining Hexokinase-2.
华蟾素通过抑制己糖激酶-2来抑制肝癌细胞的肿瘤生长并干扰其葡萄糖代谢。
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Dietary essential amino acids restore liver metabolism in ovariectomized mice via hepatic estrogen receptor α.饮食必需氨基酸通过肝脏雌激素受体 α 恢复去卵巢小鼠的肝脏代谢。
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