Evidence map›Paper›PMID 39283311›Full record

ArticleThe Journal of cell biology2024

Migfilin promotes autophagic flux through direct interaction with SNAP29 and Vamp8.

Renwei Cai, Panzhu Bai, Meiling Quan, Yanyan Ding, Wenjie Wei, Chengmin Liu, Aihua Yang, Zailin Xiong, Guizhen Li, Binbin Li and 5 more

Abstract read
In one paragraph

Article in The Journal of cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

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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

15 authors.

Renwei CaiDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0001-6327-4023
Panzhu BaiDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0009-0001-0877-0400
Meiling QuanDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0009-0004-7234-6323
Yanyan DingDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0009-0005-6858-6874
Wenjie WeiDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0002-5053-791X
Chengmin LiuDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0002-0882-582X
Aihua YangDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0009-0005-6406-3590
Zailin XiongDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0009-0005-5426-8138
Guizhen LiDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0009-0009-3546-3850
Binbin LiDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0009-0006-7916-3006
Yi DengDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0003-1378-015X
Ruijun TianDepartment of Chemistry, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0001-9521-5124
Yan G ZhaoDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0002-4588-6752
Chuanyue WuDepartment of Pathology, School of Medicine and University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA.ORCID 0000-0003-2536-4014
Ying SunDepartment of System Biology, School of Life Sciences, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0001-6706-5720

Funding

National Natural Science Foundation of China 8237100185Natural Science Foundation of Guangdong Province 2024A1515013048Shenzhen Innovation Committee of Science and Technology JCYJ20200109141212325
6 · The paper itself

Abstract

Autophagy plays a crucial role in cancer cell survival by facilitating the elimination of detrimental cellular components and the recycling of nutrients. Understanding the molecular regulation of autophagy is critical for developing interventional approaches for cancer therapy. In this study, we report that migfilin, a focal adhesion protein, plays a novel role in promoting autophagy by increasing autophagosome-lysosome fusion. We found that migfilin is associated with SNAP29 and Vamp8, thereby facilitating Stx17-SNAP29-Vamp8 SNARE complex assembly. Depletion of migfilin disrupted the formation of the SNAP29-mediated SNARE complex, which consequently blocked the autophagosome-lysosome fusion, ultimately suppressing cancer cell growth. Restoration of the SNARE complex formation rescued migfilin-deficiency-induced autophagic flux defects. Finally, we found depletion of migfilin inhibited cancer cell proliferation. SNARE complex reassembly successfully reversed migfilin-deficiency-induced inhibition of cancer cell growth. Taken together, our study uncovers a new function of migfilin as an autophagy-regulatory protein and suggests that targeting the migfilin-SNARE assembly could provide a promising therapeutic approach to alleviate cancer progression.

Indexed as

AutophagyCell Adhesion MoleculesCell ProliferationLysosomesQb-SNARE ProteinsQc-SNARE ProteinsR-SNARE ProteinsAutophagosomesCell Line, TumorHeLa CellsHumansMembrane FusionProtein BindingQa-SNARE ProteinsSNARE ProteinsCell Adhesion MoleculesQa-SNARE ProteinsQb-SNARE ProteinsQc-SNARE ProteinsR-SNARE ProteinsSNAP29 protein, humanSNARE ProteinsSTX17 protein, humanVAMP8 protein, human

Identifiers

PMID39283311
PMCPMC11404564

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

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.