Evidence map›Paper›PMID 31320625›Full record

ArticleNature communications2019

PRKCSH contributes to tumorigenesis by selective boosting of IRE1 signaling pathway.

Gu-Choul Shin, Sung Ung Moon, Hong Seok Kang, Hyo-Sun Choi, Hee Dong Han, Kyun-Hwan Kim

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 41 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Gu-Choul ShinDepartment of Pharmacology, Center for Cancer Research and Diagnostic Medicine, IBST, School of Medicine, Konkuk University, 1 Hwayang-Dong, Kwangjin-Gu, Seoul, 143-701, Republic of Korea. rnelr@naver.com.ORCID http://orcid.org/0000-0001-8200-9700
Sung Ung MoonCenter for Advanced Bioinformatics & Systems Medicine, Sookmyung Women's University, Hyochangwon-Gil 52, Youngsan-Gu, Seoul, 140-741, Republic of Korea.
Hong Seok KangDepartment of Pharmacology, Center for Cancer Research and Diagnostic Medicine, IBST, School of Medicine, Konkuk University, 1 Hwayang-Dong, Kwangjin-Gu, Seoul, 143-701, Republic of Korea.
Hyo-Sun ChoiDepartment of Pharmacology, Center for Cancer Research and Diagnostic Medicine, IBST, School of Medicine, Konkuk University, 1 Hwayang-Dong, Kwangjin-Gu, Seoul, 143-701, Republic of Korea.
Hee Dong HanDepartment of Immunology, School of Medicine, Konkuk University, Chungwon-Daero 268, Chungju, Republic of Korea.
Kyun-Hwan KimDepartment of Pharmacology, Center for Cancer Research and Diagnostic Medicine, IBST, School of Medicine, Konkuk University, 1 Hwayang-Dong, Kwangjin-Gu, Seoul, 143-701, Republic of Korea. khkim10@kku.ac.kr.ORCID http://orcid.org/0000-0001-5266-072X
Konkuk University · KRSookmyung Women's University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unfolded protein response (UPR) is an adaptive mechanism that aims at restoring ER homeostasis under severe environmental stress. Malignant cells are resistant to environmental stress, which is largely due to an activated UPR. However, the molecular mechanisms by which different UPR branches are selectively controlled in tumor cells are not clearly understood. Here, we provide evidence that PRKCSH, previously known as glucosidase II beta subunit, functions as a regulator for selective activation of the IRE1α branch of UPR. PRKCSH boosts ER stress-mediated autophosphorylation and oligomerization of IRE1α through mutual interaction. PRKCSH contributes to the induction of tumor-promoting factors and to tumor resistance to ER stress. Increased levels of PRKCSH in various tumor tissues are positively correlated with the expression of XBP1-target genes. Taken together, our data provide a molecular rationale for selective activation of the IRE1α branch in tumors and adaptation of tumor cells to severe environmental stress.

Indexed as

AnimalsCalcium-Binding ProteinsCell Line, TumorCell SurvivalCell Transformation, NeoplasticEndoplasmic Reticulum StressEndoribonucleasesGlucosidasesHep G2 CellsHumansMaleMiceMice, Inbred BALB CNeoplasmsProtein Serine-Threonine KinasesRNA InterferenceCalcium-Binding ProteinsEndoribonucleasesERN1 protein, humanGlucosidasesPRKCSH protein, humanProtein Serine-Threonine KinasesRNA, Small Interfering

Identifiers

PMID31320625
PMCPMC6639383
OpenAlexW2961758828

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.