Evidence map›Paper›PMID 26942872›Full record

ArticleOncotarget2016

APIP, an ERBB3-binding partner, stimulates erbB2-3 heterodimer formation to promote tumorigenesis.

Se-Hoon Hong, Won Jae Lee, Young Doo Kim, Hyunjoo Kim, Young-Jun Jeon, Bitna Lim, Dong-Hyung Cho, Won Do Heo, Doo-Hyun Yang, Chan-Young Kim and 3 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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

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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

13 authors at 5 institutions in 1 country.

Se-Hoon HongSchool of Biological Science, Seoul National University, Gwanak-gu, Seoul 151-747, Korea.
Won Jae LeeSchool of Biological Science, Seoul National University, Gwanak-gu, Seoul 151-747, Korea.
Young Doo KimSchool of Biological Science, Seoul National University, Gwanak-gu, Seoul 151-747, Korea.
Hyunjoo KimSchool of Biological Science, Seoul National University, Gwanak-gu, Seoul 151-747, Korea.
Young-Jun JeonSchool of Biological Science, Seoul National University, Gwanak-gu, Seoul 151-747, Korea.
Bitna LimSchool of Biological Science, Seoul National University, Gwanak-gu, Seoul 151-747, Korea.
Dong-Hyung ChoGraduate School of East-West Medical Science, Kyung Hee University, Gyeoggi-Do 446-701, Korea.
Won Do HeoDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Doo-Hyun YangDepartment of Surgery, Chonbuk National University Medical School, Jeonju 561-180, Korea.
Chan-Young KimDepartment of Surgery, Chonbuk National University Medical School, Jeonju 561-180, Korea.
Han-Kwang YangDepartment of Surgery, Seoul National University College of Medicine, Seoul 110-744, Korea.
Jin Kuk YangDepartment of Chemistry, College of Natural Sciences, Soongsil University, Seoul 156-743, Korea.
Yong-Keun JungSchool of Biological Science, Seoul National University, Gwanak-gu, Seoul 151-747, Korea.
Seoul National University · KRJeonbuk National University · KRKorea Advanced Institute of Science and Technology · KRKyung Hee University · KRSoongsil University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the fact that the epidermal growth factor (EGF) family member ERBB3 (HER3) is deregulated in many cancers, the list of ERBB3-interacting partners remains limited. Here, we report that the Apaf-1-interacting protein (APIP) stimulates heregulin-β1 (HRG-β1)/ERBB3-driven cell proliferation and tumorigenesis. APIP levels are frequently increased in human gastric cancers and gastric cancer-derived cells. Cell proliferation and tumor formation are repressed by APIP downregulation and stimulated by its overexpression. APIP's role in the ERBB3 pathway is not associated with its functions within the methionine salvage pathway. In response to HRG-β1, APIP binds to the ERBB3 receptor, leading to an enhanced binding of ERBB3 and ERBB2 that results in sustained activations of ERK1/2 and AKT protein kinases. Furthermore, HRG-β1/ERBB3-dependent signaling is gained in APIP transgenic mouse embryonic fibroblasts (MEFs), but not lost in Apip-/- MEFs. Our findings offer compelling evidence that APIP plays an essential role in ERBB3 signaling as a positive regulator for tumorigenesis, warranting future development of therapeutic strategies for ERBB3-driven gastric cancer.

Indexed as

AnimalsApoptosis Regulatory ProteinsCarcinogenesisCell Line, TumorCell ProliferationCells, CulturedErb-b2 Receptor Tyrosine KinasesFemaleHumansMaleMiceMice, KnockoutMice, NudeMice, TransgenicMiddle AgedNIH 3T3 CellsAPIP protein, humanApoptosis Regulatory ProteinsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesERBB3 protein, humanReceptor, ErbB-3APIPERBB2ERBB3gastric cancerHRG-β1

Identifiers

PMID26942872
PMCPMC5008309
OpenAlexW2291452118

What OpenQuestion holds

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LicenceCC BY
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.