Evidence map›Paper›PMID 27191259›Full record

ArticleOncotarget2016

Notch1 pathway-mediated microRNA-151-5p promotes gastric cancer progression.

Kai-Wen Hsu, Wen-Liang Fang, Kuo-Hung Huang, Tzu-Ting Huang, Hsin-Chen Lee, Rong-Hong Hsieh, Chin-Wen Chi, Tien-Shun Yeh

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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 46 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

8 authors at 4 institutions in 1 country.

Kai-Wen HsuInstitute of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Wen-Liang FangInstitute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Kuo-Hung HuangInstitute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Tzu-Ting HuangInstitute of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Hsin-Chen LeeDepartment and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Rong-Hong HsiehSchool of Nutrition and Health Sciences, College of Public Health and Nutrition, Taipei Medical University, Taipei 110, Taiwan.
Chin-Wen ChiDepartment and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Tien-Shun YehInstitute of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
National Yang Ming Chiao Tung University · TWTaipei Veterans General Hospital · TWInstitute of Molecular Biology, Academia Sinica · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric carcinoma is the third leading cause of lethal cancer worldwide. Previous studies showed that Notch1 receptor intracellular domain (N1IC), the activated form of Notch1 receptor, promotes gastric cancer progression. It has been demonstrated that a significant cross-talk interplays between Notch pathways and microRNAs (miRNAs) in controlling tumorigenesis. This study identified an intronic microRNA-151 (miR-151), which consists of two mature miRNAs, miR-151-3p and miR-151-5p, as a Notch1 receptor-induced miRNA in gastric cancer cells. Activation of Notch1 pathway enhanced expressions of miR-151 and its host gene, focal adhesion kinase (FAK), in gastric cancer cells. The levels of miR-151 in gastric cancer samples were higher than those of adjacent non-tumor samples. Activated Notch1 pathway induced CBF1-dependent FAK promoter activity. The ectopic expression of miR-151 promoted growth and progression of SC-M1 gastric cancer cells including cell viability and colony formation, migration, and invasion abilities. Activated Notch1 pathway could augment progression of gastric cancer cells through miR-151-5p and FAK. The mRNA levels of pluripotency genes, Nanog and SOX-2, tumorsphere formation ability, tumor growth, and lung metastasis of SC-M1 cells were elevated by activated Notch1 pathway through miR-151-5p. Furthermore, miR-151-5p could target 3'-untranslated region (3'-UTR) of p53 mRNA and down-regulate p53 level in SC-M1 cells. Mechanistically, Notch1/miR-151-5p axis contributed to progression of SC-M1 cells through down-regulation of p53 which in turn repressed FAK promoter activity. Taken together, these results suggest that Notch1 pathway and miR-151-5p interplay with p53 in a reciprocal regulation loop in controlling gastric carcinogenesis.

Indexed as

AnimalsCell Line, TumorDisease ProgressionFocal Adhesion Kinase 1HEK293 CellsHeterograftsHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinK562 CellsMiceMice, Inbred BALB CMice, NudeMicroRNAsPromoter Regions, GeneticReceptor, Notch1Stomach NeoplasmsFocal Adhesion Kinase 1Immunoglobulin J Recombination Signal Sequence-Binding ProteinMicroRNAsMIRN151a microRNA, humanNOTCH1 protein, humanPTK2 protein, humanRBPJ protein, humanReceptor, Notch1TP53 protein, humanTumor Suppressor Protein p53FAKgastric carcinogenesismiR-151Notch1 receptorp53

Identifiers

PMID27191259
PMCPMC5122370
OpenAlexW2368877735

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.