Evidence map›Paper›PMID 26041881›Full record

ArticleOncotarget2015

The reciprocal regulation loop of Notch2 pathway and miR-23b in controlling gastric carcinogenesis.

Tzu-Ting Huang, Yueh-Hsin Ping, An-Ming Wang, Chia-Chi Ke, Wen-Liang Fang, Kuo-Hung Huang, Hsin-Chen Lee, Chin-Wen Chi, Tien-Shun Yeh

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 46 citations in OpenAlex.

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  8. [Effect of miR-23b on the malignant phenotype and the sensitivity of lenvatinib in human hepatocellular carcinoma cells].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021
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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

9 authors at 3 institutions in 1 country.

Tzu-Ting HuangDepartment and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Yueh-Hsin PingDepartment and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
An-Ming WangDepartment of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Chia-Chi KeDepartment of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Wen-Liang FangInstitute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Kuo-Hung HuangInstitute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Hsin-Chen LeeDepartment and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Chin-Wen ChiDepartment and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Tien-Shun YehDepartment of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
National Yang Ming Chiao Tung University · TWInstitute of Molecular Biology, Academia Sinica · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric carcinoma is one of the most common malignancies and the third highest cause of global cancer-related death. Notch2 receptor intracellular domain (N2IC), the activated form of Notch2 receptor, enhances gastric carcinogenesis. MicroRNAs (miRNAs) act as either oncogenes or tumor suppressors in tumorigenesis and cross-talk with Notch pathways. Herein, microRNA-23b (miR-23b) was identified as a Notch2 receptor-related miRNA and its role in gastric carcinogenesis was investigated. Levels of miR-23b in stomach adenocarcinoma samples were down-regulated, whereas those of Notch2 receptor, v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets1), and E2F1 transcripts were up-regulated. Results also showed that N2IC down-regulated miR-23b expression in gastric cancer cells through up-regulating E2F1. The miR-23b inhibited gastric tumorigenesis including growth, viability, epithelial-mesenchymal transition, and abilities of colony formation, migration, invasion, and tumorsphere formation. Mechanistically, miR-23b suppressed tumor progression and pluripotency gene expression and affected tumorsphere ultra-structure in gastric cancer cells via targeting Notch2 receptor or Ets1. Furthermore, miR-23b diminished the xenografted tumor growth and lung metastasis of SC-M1 gastric cancer cells through Notch2 pathway. Our results suggest that Notch2 pathway and miR-23b interplay in a reciprocal regulation loop in gastric cancer cells and this axis plays an important role in gastric carcinogenesis.

Indexed as

3' Untranslated RegionsAdenocarcinomaAnimalsBinding SitesCell Line, TumorCell MovementCell ProliferationE2F1 Transcription FactorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGenetic TherapyHumansLung NeoplasmsMaleMice, Inbred BALB CMice, Inbred NOD3' Untranslated RegionsE2F1 protein, humanE2F1 Transcription FactorETS1 protein, humanMicroRNAsMIRN23a microRNA, humanNOTCH2 protein, humanProto-Oncogene Protein c-ets-1Receptor, Notch2E2F1Ets1gastric carcinogenesismiR-23bNotch2 receptor

Identifiers

PMID26041881
PMCPMC4627232
OpenAlexW1756866299

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.