Evidence map›Paper›PMID 35165763›Full record

ArticleCellular and molecular life sciences : CMLS2022

Sec62 promotes gastric cancer metastasis through mediating UPR-induced autophagy activation.

Song Su, Yan-Ting Shi, Yi Chu, Ming-Zuo Jiang, Nan Wu, Bing Xu, He Zhou, Jun-Chao Lin, Yi-Rong Jin, Xiao-Fei Li and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 29 citations in OpenAlex.

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  14. Autophagy and its role in gastrointestinal diseases.World journal of gastroenterology · 2024
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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

11 authors at 4 institutions in 1 country.

Song Su *State Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China.
Yan-Ting Shi *State Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China.
Yi ChuState Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China.
Ming-Zuo JiangState Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China.
Nan WuCollege of Life Sciences, Northwest University, Xi'an, Shaanxi, 710069, China.
Bing XuKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education. School of Medicine, Northwest University, 229 Taibai North Road, Xi'an, Shaanxi, 710069, China.
He ZhouState Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China.
Jun-Chao LinState Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China.
Yi-Rong JinState Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China.
Xiao-Fei LiState Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China.
Jie LiangState Key Laboratory of Cancer Biology and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University (Air Force Medical University), Changle West Road 127, Xi'an, Shaanxi, 710032, China. liangjie@fmmu.edu.cn.ORCID http://orcid.org/0000-0002-6792-8941
National Clinical Research Center for Digestive Diseases · CNChinese PLA General Hospital · CNMinistry of Education of the People's Republic of China · CNNorthwest University · CN

Funding

foundation for the author of national excellent doctoral dissertation of the people's republic of china 201182national natural science foundation of china 81322037national natural science foundation of china 81421003national natural science foundation of china 81572302national natural science foundation of china 81772650
6 · The paper itself

Abstract

BACKGROUND AND

aimsSec62 is a membrane protein of the endoplasmic reticulum that facilitates protein transport. Its role in cancer is increasingly recognised, but remains largely unknown. We investigated the functional role of Sec62 in gastric cancer (GC) and its underlying mechanism.

methodsBioinformatics, tissue microarray, immunohistochemistry (IHC), western blotting (WB), quantitative polymerase chain reaction (qPCR), and immunofluorescence were used to examine the expression of target genes. Transwell, scratch healing assays, and xenograft models were used to evaluate cell migration and invasion. Transmission electron microscopy and mRFP-GFP-LC3 double-labeled adenoviruses were used to monitor autophagy. Co-immunoprecipitation (CO-IP) was performed to evaluate the binding activity between the proteins.

resultsSec62 expression was upregulated in GC, and Sec62 upregulation was an independent predictor of poor prognosis. Sec62 overexpression promoted GC cell migration and invasion both in vitro and in vivo. Sec62 promoted migration and invasion by affecting TIMP-1 and MMP2/9 balance. Moreover, Sec62 could activate autophagy by upregulating PERK/ATF4 expression and binding to LC3II with concomitant FIP200/Beclin-1/Atg5 activation. Furthermore, autophagy blockage impaired the promotive effects of Sec62 on GC cell migration and invasion, whereas autophagy activation rescued the inhibitory effect of Sec62 knockdown on GC metastasis. Notably, Sec62 inhibition combined with autophagy blockage exerted a synergetic anti-metastatic effect in vitro and in vivo.

conclusionSec62 promotes GC metastasis by activating autophagy and subsequently regulating TIMP-1 and MMP2/9 balance. The activation of autophagy by Sec62 may involve the unfolded protein response (UPR)-related PERK/ATF4 pathway and binding of LC3II during UPR recovery involving FIP200/Beclin-1/Atg5 upregulation. Specifically, the dual inhibition of Sec62 and autophagy may provide a promising therapeutic strategy for GC metastasis.

Indexed as

AdultAgedAged, 80 and overAnimalsAutophagyCell Line, TumoreIF-2 KinaseFemaleHumansHydroxychloroquineMaleMatrix Metalloproteinase 2Membrane Transport ProteinsMiceMice, Inbred BALB CMiddle AgedEIF2AK3 protein, humaneIF-2 KinaseHydroxychloroquineMatrix Metalloproteinase 2Membrane Transport ProteinsSEC62 protein, humanTissue Inhibitor of Metalloproteinase-1EMTER-phagyER stressProtein translocation machineryUnfolded protein response (UPR)

Identifiers

PMID35165763
PMCPMC11073224
OpenAlexW4213178925

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.