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PGC1α缺失通过上皮-间质转化促进肺癌转移。

PGC1α Loss Promotes Lung Cancer Metastasis through Epithelial-Mesenchymal Transition.

作者信息

Oh Taek-In, Lee Mingyu, Lee Yoon-Mi, Kim Geon-Hee, Lee Daekee, You Jueng Soo, Kim Sun Ha, Choi Minyoung, Jang Hyonchol, Park Yeong-Min, Shin Hyun-Woo, Shin Dong Hoon, Lim Ji-Hong

机构信息

Department of Biomedical Chemistry, College of Biomedical & Health Science, Konkuk University, Chungju 27478, Korea.

Department of Applied Life Science, Graduate School, BK21 Program, Konkuk University, Chungju 27478, Korea.

出版信息

Cancers (Basel). 2021 Apr 8;13(8):1772. doi: 10.3390/cancers13081772.

DOI:10.3390/cancers13081772
PMID:33917757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8068195/
Abstract

PGC1α oppositely regulates cancer metastasis in melanoma, breast, and pancreatic cancer; however, little is known about its impact on lung cancer metastasis. Transcriptome and in vivo xenograft analysis show that a decreased PGC1α correlates with the epithelial-mesenchymal transition (EMT) and lung cancer metastasis. The deletion of a single Pgc1α allele in mice promotes bone metastasis of Kras-driven lung cancer. Mechanistically, PGC1α predominantly activates ID1 expression, which interferes with TCF4-TWIST1 cooperation during EMT. Bioinformatic and clinical studies have shown that PGC1α and ID1 are downregulated in lung cancer, and correlate with a poor survival rate. Our study indicates that TCF4-TWIST1-mediated EMT, which is regulated by the PGC1α-ID1 transcriptional axis, is a potential diagnostic and therapeutic target for metastatic lung cancer.

摘要

PGC1α在黑色素瘤、乳腺癌和胰腺癌中对癌症转移具有相反的调节作用；然而，其对肺癌转移的影响却知之甚少。转录组和体内异种移植分析表明，PGC1α水平降低与上皮-间质转化（EMT）及肺癌转移相关。小鼠中单个Pgc1α等位基因的缺失会促进Kras驱动的肺癌发生骨转移。从机制上讲，PGC1α主要激活ID1的表达，而ID1在EMT过程中会干扰TCF4-TWIST1的协同作用。生物信息学和临床研究表明，PGC1α和ID1在肺癌中表达下调，且与生存率低相关。我们的研究表明，由PGC1α-ID1转录轴调控的TCF4-TWIST1介导的EMT是转移性肺癌潜在的诊断和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/1b2b23eaf70a/cancers-13-01772-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/3dbeea69b429/cancers-13-01772-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/6f5ee01952a3/cancers-13-01772-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/7b1172800929/cancers-13-01772-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/24e9723355bf/cancers-13-01772-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/c98468e04b2e/cancers-13-01772-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/42b4a845ba27/cancers-13-01772-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/1b2b23eaf70a/cancers-13-01772-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/3dbeea69b429/cancers-13-01772-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/6f5ee01952a3/cancers-13-01772-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/7b1172800929/cancers-13-01772-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/24e9723355bf/cancers-13-01772-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/c98468e04b2e/cancers-13-01772-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/42b4a845ba27/cancers-13-01772-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e7/8068195/1b2b23eaf70a/cancers-13-01772-g007a.jpg

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