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Extracellular vesicles in fatty liver promote a metastatic tumor microenvironment

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单位： [1]Karsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA [2]Division of Hematology and Oncology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA [3]Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA [4]Department of Pathology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA [5]Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA [6]Department of Pathology, Veterans Affairs Greater Los Angeles Health Care System, Los Angeles, CA 90073, USA [7]Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China [8]Division of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030 China [9]Department of Pharmacy, Kangwon National University, Chuncheon 24341, South Korea [10]Houston Methodist Hospital, Houston Research Institute, Houston, TX 77030, USA

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Liver metastasis is a major cause of death in patients with colorectal cancer (CRC). Fatty liver promotes liver metastasis, but the underlying mechanism remains unclear. We demonstrated that hepatocyte-derived extracellular vesicles (EVs) in fatty liver enhanced the progression of CRC liver metastasis by promoting oncogenic Yes-associated protein (YAP) signaling and an immunosuppressive microenvironment. Fatty liver upregulated Rab27a expression, which facilitated EV production from hepatocytes. In the liver, these EVs transferred YAP signaling-regulating microRNAs to cancer cells to augment YAP activity by suppressing LATS2. Increased YAP activity in CRC liver metastasis with fatty liver promoted cancer cell growth and an immunosuppressive microenvironment by M2 macrophage infiltration through CYR61 production. Patients with CRC liver metastasis and fatty liver had elevated nuclear YAP expression, CYR61 expression, and M2 macrophage infiltration. Our data indicate that fatty liver-induced EV-microRNAs, YAP signaling, and an immunosuppressive microenvironment promote the growth of CRC liver metastasis.Copyright © 2023 Elsevier Inc. All rights reserved.

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出版当年[2022]版：

大类 | 1 区

生物学

小类 | 1 区细胞生物学 1 区内分泌学与代谢

最新[2025]版：

大类 | 1 区

生物学

小类 | 1 区细胞生物学 1 区内分泌学与代谢

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出版当年[2021]版：

Q1 CELL BIOLOGY Q1 ENDOCRINOLOGY & METABOLISM

最新[2023]版：

Q1 CELL BIOLOGY Q1 ENDOCRINOLOGY & METABOLISM

影响因子： 27.7 最新[2023版] 31.2 最新五年平均 31.373 出版当年[2021版] 35.104 出版当年五年平均 27.287 出版前一年[2020版] 29 出版后一年[2022版]

第一作者：

第一作者单位： [1]Karsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA [7]Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

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通讯作者：

通讯机构： [1]Karsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA [5]Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA

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