Evidence map›Paper›PMID 28176801›Full record

ArticleScientific reports2017

MFN2 suppresses cancer progression through inhibition of mTORC2/Akt signaling.

Ke Xu, Guo Chen, Xiaobo Li, Xiaoqin Wu, Zhijie Chang, Jianhua Xu, Yu Zhu, Peihao Yin, Xin Liang, Lei Dong

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
5.7field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

81 citing papers in PubMed, 158 citations in OpenAlex.

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  11. The Role of N6-Methyladenosine in Mitochondrial Dysfunction and Pathology.International journal of molecular sciences · 2025
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21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 8 institutions in 2 countries.

Ke XuCentral laboratory, General Surgery, Putuo Hospital, and Interventional Cancer Institute of Chinese Integrative Medicine, Shanghai University of Traditional Chinese Medicine, 164 Lanxi Rd, Shanghai 200062, PR China.
Guo ChenWinship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA.
Xiaobo LiTianjin Key Laboratory of Molecular Design and Drug Discovery, Tianjin Institute of Pharmaceutical Research, Tianjin 300193, China.
Xiaoqin WuSchool of Pharmacy, Institute for Liver Diseases of Anhui Medical University, ILDAMU, Key Laboratory of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, China.
Zhijie ChangState Key Laboratory of Membrane Biology, School of Medicine, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Jianhua XuCentral laboratory, General Surgery, Putuo Hospital, and Interventional Cancer Institute of Chinese Integrative Medicine, Shanghai University of Traditional Chinese Medicine, 164 Lanxi Rd, Shanghai 200062, PR China.
Yu ZhuDepartment of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration, Tianjin 300350, China.
Peihao YinCentral laboratory, General Surgery, Putuo Hospital, and Interventional Cancer Institute of Chinese Integrative Medicine, Shanghai University of Traditional Chinese Medicine, 164 Lanxi Rd, Shanghai 200062, PR China.
Xin LiangState Key Laboratory of Bioreactor Engineering &Shanghai Key Laboratory of New drug design, School of pharmacy, East China University of Science and Technology, 130 Meilong Rd, Shanghai 200237, PR China.
Lei DongCentral laboratory, General Surgery, Putuo Hospital, and Interventional Cancer Institute of Chinese Integrative Medicine, Shanghai University of Traditional Chinese Medicine, 164 Lanxi Rd, Shanghai 200062, PR China.
Shanghai University of Traditional Chinese Medicine · CNAnhui Medical University · CNChildren's Healthcare of Atlanta · USEast China University of Science and Technology · CNEmory University · USTianjin Huanhu Hospital · CNTianjin Institute of Pharmaceutical Research (China) · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitochondrial GTPase mitofusin-2 (MFN2) has previously been reported to play a role in regulating cell proliferation, apoptosis and differentiation in a number of cell types. Here, we report that breast cancer patients with low MFN2 expression are associated with poor prognosis as compared to patients with high MFN2 expression. We find that MFN2 knockout from MCF7 and A549 cells via Crispr/Cas9 greatly promotes cell viability, colony formation, and invasion of cancer cells in vitro and in vivo, which were confirmed by colony formation assay, transwell invasion assay, and tumor xenograft model. Signaling analyses suggest the mammalian target of rapamycin complex 2 (mTORC2)/Akt signaling pathway is highly elevated in MFN2 knockout cancer cells. The elevated mTORC2 promotes cancer cell growth and metastasis via Akt

Indexed as

Signal TransductionAnimalsCell Line, TumorDisease Models, AnimalDisease ProgressionGene ExpressionGene Knockout TechniquesGTP PhosphohydrolasesHeterograftsHumansKaplan-Meier EstimateMaleMechanistic Target of Rapamycin Complex 2Melanoma, ExperimentalMiceMitochondrial ProteinsGTP PhosphohydrolasesMechanistic Target of Rapamycin Complex 2MFN2 protein, humanMitochondrial ProteinsProto-Oncogene Proteins c-aktRapamycin-Insensitive Companion of mTOR ProteinRICTOR protein, human

Identifiers

PMID28176801
PMCPMC5296837
OpenAlexW2586923100

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.