Evidence map›Paper›PMID 27588471›Full record

ArticleOncotarget2016

Endoplasmic reticulum-Golgi intermediate compartment protein 3 knockdown suppresses lung cancer through endoplasmic reticulum stress-induced autophagy.

Seong-Ho Hong, Seung-Hee Chang, Kyung-Cho Cho, Sanghwa Kim, Sungjin Park, Ah Young Lee, Hu-Lin Jiang, Hyeon-Jeong Kim, Somin Lee, Kyeong-Nam Yu and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  8. Unlocking Golgi: Why Does Morphology Matter?Biochemistry. Biokhimiia · 2019
    Review
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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 at 6 institutions in 2 countries.

Seong-Ho HongLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Seung-Hee ChangLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Kyung-Cho ChoDepartment of Applied Chemistry, College of Applied Science, Kyung Hee University, Yongin 17104, Korea.
Sanghwa KimLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Sungjin ParkLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Ah Young LeeLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Hu-Lin JiangDepartment of Pharmaceutics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, PR China.
Hyeon-Jeong KimLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Somin LeeLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Kyeong-Nam YuLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Hwi Won SeoLaboratory of Pathology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Chanhee ChaeLaboratory of Pathology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Kwang Pyo KimDepartment of Applied Chemistry, College of Applied Science, Kyung Hee University, Yongin 17104, Korea.
Jongsun ParkDepartment of Pharmacology and Medical Science, Infection Signaling Network Research Center, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Myung-Haing ChoLaboratory of Toxicology, BK21 PLUS Program for Creative Veterinary Science Research, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Seoul National University · KRKyung Hee University · KRAdvanced Institute of Convergence Technology · KRChina Pharmaceutical University · CNChungnam National University · KRDaegu-Gyeongbuk Medical Innovation Foundation · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trafficking from the endoplasmic reticulum (ER) to the Golgi apparatus is elevated in cancer cells. Therefore, proteins of the ER-Golgi intermediate compartment (ERGIC) attract significant attention as targets for cancer treatment. Enhanced cancer cell growth and epithelial-mesenchymal transition by ERGICs correlates with poor-prognosis of lung cancer. This prompted us to assess whether knockdown of ERGIC3 may decrease lung cancer growth. To test the hypothesis, the effects of ERGIC3 short hairpin RNA (shERGIC3) on ER stress-induced cell death and lung tumorigenesis were investigated both in vitro and in vivo. Knockdown of ERGIC3 led to ER stress-induced autophagic cell death and suppression of proliferation in the A549 human lung cancer cell-line. Moreover, non-invasive aerosol-delivery of shERGIC3 using the biocompatible carrier glycerol propoxylate triacrylate and spermine (GPT-SPE) inhibited lung tumorigenesis in the K-rasLA1 murine model of lung cancer. Our data suggest that suppression of ERGIC3 could provide a framework for the development of effective lung cancer therapies.

Indexed as

Endoplasmic Reticulum StressA549 CellsAdenocarcinomaAnimalsAutophagyCarcinogenesisCell Growth ProcessesEpithelial-Mesenchymal TransitionGenes, rasHumansLungLung NeoplasmsMaleMembrane ProteinsMiceMice, TransgenicERGIC3 protein, humanMembrane ProteinsProto-Oncogene Proteins c-aktRNA, Small Interferingendoplasmic reticulum-Golgi intermediate compartment protein 3 (ERGIC3)ER stressgene therapygolgi apparatuslung cancer

Identifiers

PMID27588471
PMCPMC5323159
OpenAlexW2512443872

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.