PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer
Abstract Abnormal angiogenesis occurs during the growth of solid tumors resulting in increased vascular permeability to fluids and metastatic cancer cells. Anti-angiogenesis therapy for solid tumors is effective in the treatment of cancer patients. However, the efficacy of anti-angiogenesis therapy...
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Nature Publishing Group
2021
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oai:doaj.org-article:07436146f32043ab840f3eddf1e19e602021-11-14T12:07:01ZPRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer10.1038/s41419-021-04352-w2041-4889https://doaj.org/article/07436146f32043ab840f3eddf1e19e602021-11-01T00:00:00Zhttps://doi.org/10.1038/s41419-021-04352-whttps://doaj.org/toc/2041-4889Abstract Abnormal angiogenesis occurs during the growth of solid tumors resulting in increased vascular permeability to fluids and metastatic cancer cells. Anti-angiogenesis therapy for solid tumors is effective in the treatment of cancer patients. However, the efficacy of anti-angiogenesis therapy is limited by drug resistance. The findings of the current study showed that HIF1α R282 is methylated by PRMT3, which is necessary for its stabilization and oncogene function. Analysis showed that PRMT3-mediated tumorigenesis is HIF1α methylation-dependent. A novel therapeutic molecule (MPG-peptide) was used to inhibit HIF1α expression. These findings provided information on PRMT3 signaling pathway and HIF1/VEGFA signaling pathway and offer a novel therapeutic strategy for colorectal cancer, mainly for treatment of anti-angiogenesis resistance patients.Xin ZhangKexin WangXingbo FengJian WangYali ChuChunmeng JiaQingsi HeCheng ChenNature Publishing GrouparticleCytologyQH573-671ENCell Death and Disease, Vol 12, Iss 11, Pp 1-13 (2021) |
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DOAJ |
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EN |
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Cytology QH573-671 |
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Cytology QH573-671 Xin Zhang Kexin Wang Xingbo Feng Jian Wang Yali Chu Chunmeng Jia Qingsi He Cheng Chen PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer |
description |
Abstract Abnormal angiogenesis occurs during the growth of solid tumors resulting in increased vascular permeability to fluids and metastatic cancer cells. Anti-angiogenesis therapy for solid tumors is effective in the treatment of cancer patients. However, the efficacy of anti-angiogenesis therapy is limited by drug resistance. The findings of the current study showed that HIF1α R282 is methylated by PRMT3, which is necessary for its stabilization and oncogene function. Analysis showed that PRMT3-mediated tumorigenesis is HIF1α methylation-dependent. A novel therapeutic molecule (MPG-peptide) was used to inhibit HIF1α expression. These findings provided information on PRMT3 signaling pathway and HIF1/VEGFA signaling pathway and offer a novel therapeutic strategy for colorectal cancer, mainly for treatment of anti-angiogenesis resistance patients. |
format |
article |
author |
Xin Zhang Kexin Wang Xingbo Feng Jian Wang Yali Chu Chunmeng Jia Qingsi He Cheng Chen |
author_facet |
Xin Zhang Kexin Wang Xingbo Feng Jian Wang Yali Chu Chunmeng Jia Qingsi He Cheng Chen |
author_sort |
Xin Zhang |
title |
PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer |
title_short |
PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer |
title_full |
PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer |
title_fullStr |
PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer |
title_full_unstemmed |
PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer |
title_sort |
prmt3 promotes tumorigenesis by methylating and stabilizing hif1α in colorectal cancer |
publisher |
Nature Publishing Group |
publishDate |
2021 |
url |
https://doaj.org/article/07436146f32043ab840f3eddf1e19e60 |
work_keys_str_mv |
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_version_ |
1718429387623235584 |