Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathway

Abstract Objective Mitochondrial fission regulator 2 (MTFR2) is upregulated in multiple cancers, including hepatocellular carcinoma (HCC); however, its mechanistic role in HCC progression remains poorly understood. Methods MTFR2 expression in HCC tissues was analyzed using TCGA and GEO databases. Va...

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Main Authors: Qiang Sun, Kaikun Liu, Fangjie Zheng, Xinwei Chen
Format: Article
Language:English
Published: BMC 2025-06-01
Series:Cell Division
Subjects:
Online Access:https://doi.org/10.1186/s13008-025-00160-2
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author Qiang Sun
Kaikun Liu
Fangjie Zheng
Xinwei Chen
author_facet Qiang Sun
Kaikun Liu
Fangjie Zheng
Xinwei Chen
author_sort Qiang Sun
collection DOAJ
description Abstract Objective Mitochondrial fission regulator 2 (MTFR2) is upregulated in multiple cancers, including hepatocellular carcinoma (HCC); however, its mechanistic role in HCC progression remains poorly understood. Methods MTFR2 expression in HCC tissues was analyzed using TCGA and GEO databases. Validation of MTFR2 expression levels in clinical samples and HCC cell lines was performed through qRT-PCR and western blot. Functional effects of MTFR2 overexpression and knockdown on HCC cell proliferation, migration, and invasion were assessed via CCK-8, colony formation, wound healing, and transwell assays. In vivo tumor growth was evaluated in xenograft mouse models. Results MTFR2 was significantly overexpressed in HCC tissues and cell lines. Enhanced proliferation, migration, invasion, and colony formation were observed in MTFR2-overexpressing HCC cells, whereas knockdown of MTFR2 suppressed these malignant phenotypes. Mechanistic studies demonstrated that MTFR2 promotes proliferation, migration, and invasion of HCC cells via the PI3K/AKT signaling pathway. Additionally, MTFR2 knockdown significantly attenuated tumor growth in xenograft models. Conclusion These findings demonstrate that MTFR2 promotes HCC progression via modulation of the PI3K/AKT pathway, underscoring its potential as a therapeutic target for HCC.
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institution Kabale University
issn 1747-1028
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publishDate 2025-06-01
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series Cell Division
spelling doaj-art-5cb99f37de1a4e6b8bcbb63d3198d0ff2025-08-20T03:31:41ZengBMCCell Division1747-10282025-06-0120111110.1186/s13008-025-00160-2Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathwayQiang Sun0Kaikun Liu1Fangjie Zheng2Xinwei Chen3Department of General Surgery, HangZhou First People′s Hospital. TongLu CampusDepartment of General Surgery, HangZhou First People′s Hospital. TongLu CampusDepartment of General Surgery, HangZhou First People′s Hospital. TongLu CampusDepartment of General Surgery, HangZhou First People′s Hospital. TongLu CampusAbstract Objective Mitochondrial fission regulator 2 (MTFR2) is upregulated in multiple cancers, including hepatocellular carcinoma (HCC); however, its mechanistic role in HCC progression remains poorly understood. Methods MTFR2 expression in HCC tissues was analyzed using TCGA and GEO databases. Validation of MTFR2 expression levels in clinical samples and HCC cell lines was performed through qRT-PCR and western blot. Functional effects of MTFR2 overexpression and knockdown on HCC cell proliferation, migration, and invasion were assessed via CCK-8, colony formation, wound healing, and transwell assays. In vivo tumor growth was evaluated in xenograft mouse models. Results MTFR2 was significantly overexpressed in HCC tissues and cell lines. Enhanced proliferation, migration, invasion, and colony formation were observed in MTFR2-overexpressing HCC cells, whereas knockdown of MTFR2 suppressed these malignant phenotypes. Mechanistic studies demonstrated that MTFR2 promotes proliferation, migration, and invasion of HCC cells via the PI3K/AKT signaling pathway. Additionally, MTFR2 knockdown significantly attenuated tumor growth in xenograft models. Conclusion These findings demonstrate that MTFR2 promotes HCC progression via modulation of the PI3K/AKT pathway, underscoring its potential as a therapeutic target for HCC.https://doi.org/10.1186/s13008-025-00160-2Hepatocellular carcinoma (HCC)Mitochondrial fission regulator 2 (MTFR2)ProliferationInvasionPI3K/AKT
spellingShingle Qiang Sun
Kaikun Liu
Fangjie Zheng
Xinwei Chen
Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathway
Cell Division
Hepatocellular carcinoma (HCC)
Mitochondrial fission regulator 2 (MTFR2)
Proliferation
Invasion
PI3K/AKT
title Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathway
title_full Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathway
title_fullStr Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathway
title_full_unstemmed Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathway
title_short Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathway
title_sort mitochondrial fission regulator 2 promotes cell proliferation migration and invasion in hepatocellular carcinoma through regulating pi3k akt signaling pathway
topic Hepatocellular carcinoma (HCC)
Mitochondrial fission regulator 2 (MTFR2)
Proliferation
Invasion
PI3K/AKT
url https://doi.org/10.1186/s13008-025-00160-2
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AT fangjiezheng mitochondrialfissionregulator2promotescellproliferationmigrationandinvasioninhepatocellularcarcinomathroughregulatingpi3kaktsignalingpathway
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