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FAM84B 在胰腺导管腺癌中扩增，通过 Wnt/β-catenin 通路促进肿瘤发生。

FAM84B, amplified in pancreatic ductal adenocarcinoma, promotes tumorigenesis through the Wnt/β-catenin pathway.

机构信息

Department of Gastrointestinal surgery, Changhai Hospital, Second Military Medical University, Yangpu 200433, Shanghai, China.

Department of Gastrointestinal Surgery, Changzheng Hospital, Second Military Medical University, Huangpu 200003, Shanghai, China.

出版信息

Aging (Albany NY). 2020 Apr 14;12(8):6808-6822. doi: 10.18632/aging.103044.

DOI:10.18632/aging.103044
PMID:32291380
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7202512/
Abstract

Altered expression of family with sequence similarity 84, member B (FAM84B) has been found in various human cancers. However, the expression and function of FAM84B in pancreatic ductal adenocarcinoma (PDAC) has not been studied. Here, by analyzing The Cancer Genome Atlas cohort, we found that amplification was observed in 11% of 141 PDAC patients, and amplification was correlated with higher mRNA expression of FAM84B. amplification and overexpression was significantly correlated with poor overall survival. Moreover, knockdown of FAM84B in PDAC cell lines suppressed cell proliferation and induced apoptosis. FAM84B knockdown also suppressed mitochondrial function and glycolysis of PDAC cells. Interestingly, knockdown of FAM84B decreased the nuclear accumulation of β-catenin, and the expression of c-Myc and lactate dehydrogenase A, but enhanced the expression of Survivin. On the contrary, FAM84B overexpression displayed reversed effects in cell proliferation, apoptosis, mitochondrial function, and glycolysis, which was blocked by the Wnt/β-catenin pathway inhibitor (XAV939). In addition, PDAC cells with lower expression of FAM84B were more sensitive to gemcitabine-induced cell proliferation inhibition both and . In conclusion, FAM84B plays an important role in aerobic glycolysis and tumorigenesis in PDAC and Wnt/β-catenin may be involved in this process.

摘要

家族与序列相似性 84 成员 B（FAM84B）的表达改变已在各种人类癌症中发现。然而，FAM84B 在胰腺导管腺癌（PDAC）中的表达和功能尚未研究。在这里，通过分析癌症基因组图谱队列，我们发现 141 例 PDAC 患者中有 11%观察到扩增，并且扩增与 FAM84B 的高 mRNA 表达相关。扩增和过表达与总体生存不良显著相关。此外，PDAC 细胞系中 FAM84B 的敲低抑制了细胞增殖并诱导了细胞凋亡。FAM84B 敲低还抑制了 PDAC 细胞的线粒体功能和糖酵解。有趣的是，FAM84B 的敲低降低了 β-连环蛋白的核积累，以及 c-Myc 和乳酸脱氢酶 A 的表达，但增强了 Survivin 的表达。相反，FAM84B 的过表达在细胞增殖、凋亡、线粒体功能和糖酵解中表现出相反的效果，这被 Wnt/β-连环蛋白通路抑制剂（XAV939）阻断。此外，FAM84B 表达较低的 PDAC 细胞对吉西他滨诱导的细胞增殖抑制更敏感，无论是 和 。总之，FAM84B 在 PDAC 的有氧糖酵解和肿瘤发生中发挥重要作用，Wnt/β-连环蛋白可能参与这一过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/5284531e15b9/aging-12-103044-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/7566f4e2eb81/aging-12-103044-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/2f0bbebeec30/aging-12-103044-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/d7c8648c805c/aging-12-103044-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/7a4a76cd12d8/aging-12-103044-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/89bd27e368d3/aging-12-103044-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/5284531e15b9/aging-12-103044-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/7566f4e2eb81/aging-12-103044-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/2f0bbebeec30/aging-12-103044-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/d7c8648c805c/aging-12-103044-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/7a4a76cd12d8/aging-12-103044-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/89bd27e368d3/aging-12-103044-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/7202512/5284531e15b9/aging-12-103044-g006.jpg

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