Evidence map›Paper›PMID 26775697›Full record

ArticleCell death & disease2016

EMC6/TMEM93 suppresses glioblastoma proliferation by modulating autophagy.

X Shen, S Kan, J Hu, M Li, G Lu, M Zhang, S Zhang, Y Hou, Y Chen, Y Bai

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  5. EMC3 is critical for CFTR function and calcium mobilization in the mouse intestinal epithelium.American journal of physiology. Gastrointestinal and liver physiology · 2025
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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

10 authors at 2 institutions in 2 countries.

X ShenDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
S KanDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
J HuKey Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing, China.
M LiDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
G LuDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
M ZhangDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
S ZhangDepartment of Cardiology, Peking University Third Hospital, Beijing, China.
Y HouDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Y ChenKey Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing, China.
Y BaiDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Peking University · CNNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EMC6 (endoplasmic reticulum membrane protein complex subunit 6), also known as transmembrane protein 93, is a novel positive autophagy regulator. In this report, we evaluated the anti-tumor activity of EMC6 in glioblastoma cells in vitro and in vivo. Our data show that overexpression of EMC6 in three glioblastoma cell lines (SHG44, U87 and U251) suppresses tumor cell growth by activating autophagy, but fails to induce cell apoptosis. EMC6-mediated autophagy was associated with inactivation of the PIK3CA/AKT/mTOR signaling pathway. Accordingly, EMC6 knockdown in glioblastoma cells had the opposite effect; it promoted cell growth. Overexpression of EMC6 also sensitized glioblastoma cells to the chemotherapy drug, temozolomide, to further suppress tumor growth. Our data indicate that EMC6-induced autophagy may play a positive role in suppressing the development of glioblastoma.

Indexed as

AnimalsAutophagyCell Line, TumorCell ProliferationEndoplasmic ReticulumGlioblastomaHumansMembrane ProteinsMiceMice, Inbred BALB CMice, NudeSignal TransductionEMC6 protein, humanMembrane Proteins

Identifiers

PMID26775697
PMCPMC4816184
OpenAlexW2415546912

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.