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タイトル: | ASPSCR1::TFE3 orchestrates the angiogenic program of alveolar soft part sarcoma |
著者: | Tanaka, Miwa Chuaychob, Surachada https://orcid.org/0000-0003-3368-9951 (unconfirmed) Homme, Mizuki Yamazaki, Yukari Lyu, Ruyin Yamashita, Kyoko Ae, Keisuke Matsumoto, Seiichi Kumegawa, Kohei Maruyama, Reo Qu, Wei Miyagi, Yohei Yokokawa, Ryuji https://orcid.org/0000-0002-6306-2693 (unconfirmed) Nakamura, Takuro |
著者名の別形: | 田中, 美和 本目, みずき 山崎, ゆかり 山下, 享子 阿江, 啓介 松本, 誠一 粂川, 昂平 丸山, 玲緒 宮城, 洋平 横川, 隆司 中村, 卓郎 |
キーワード: | Cancer models Epigenomics Sarcoma Small GTPases Tumour angiogenesis |
発行日: | 7-Apr-2023 |
出版者: | Springer Nature |
誌名: | Nature Communications |
巻: | 14 |
論文番号: | 1957 |
抄録: | Alveolar soft part sarcoma (ASPS) is a soft part malignancy affecting adolescents and young adults. ASPS is characterized by a highly integrated vascular network, and its high metastatic potential indicates the importance of ASPS’s prominent angiogenic activity. Here, we find that the expression of ASPSCR1::TFE3, the fusion transcription factor causatively associated with ASPS, is dispensable for in vitro tumor maintenance; however, it is required for in vivo tumor development via angiogenesis. ASPSCR1::TFE3 is frequently associated with super-enhancers (SEs) upon its DNA binding, and the loss of its expression induces SE-distribution dynamic modification related to genes belonging to the angiogenesis pathway. Using epigenomic CRISPR/dCas9 screening, we identify Pdgfb, Rab27a, Sytl2, and Vwf as critical targets associated with reduced enhancer activities due to the ASPSCR1::TFE3 loss. Upregulation of Rab27a and Sytl2 promotes angiogenic factor-trafficking to facilitate ASPS vascular network construction. ASPSCR1::TFE3 thus orchestrates higher ordered angiogenesis via modulating the SE activity. |
記述: | がんにおける新たな血管新生機構を発見 --肉腫の融合遺伝子とその標的分子の機能を明らかにする--. 京都大学プレスリリース. 2023-04-11. |
著作権等: | © The Author(s) 2023 This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. |
URI: | http://hdl.handle.net/2433/281588 |
DOI(出版社版): | 10.1038/s41467-023-37049-z |
PubMed ID: | 37029109 |
関連リンク: | https://www.t.kyoto-u.ac.jp/ja/research/topics/20230411 |
出現コレクション: | 学術雑誌掲載論文等 |
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