Evidence map›Paper›PMID 27733214›Full record

ArticleOncology research2017

miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1.

Sheqing Ji, Bin Zhang, Ye Kong, Fei Ma, Yawei Hua

Abstract read
In one paragraph

Article in Oncology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
–field-weighted citation impact
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

48 citing papers in PubMed.

  1. International journal of breast cancer · 2026
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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

5 authors.

Sheqing Ji
Bin Zhang
Ye Kong
Fei Ma
Yawei Hua

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) play a crucial role in the development and progression of human cancers, including gastric cancer (GC). The discovery of miRNAs may provide a new and powerful tool for studying the mechanism, diagnosis, and treatment of GC. In this study, we aimed to investigate the role of miR-326 in the development and progression of GC. Quantitative PCR (qPCR) was used to measure the expression level of miR-326 in GC tissues and cell lines. We found that miR-326 was significantly downregulated during GC. In addition, overexpression of miR-326 inhibited GC cell proliferation. Fluorescence-activated cell sorting (FACS) further showed that miR-326 significantly induced GC cell G2/M arrest. Subsequent dual-luciferase reporter assay identified one of the proto-oncogene NOB1 as a direct target of miR-326, and NOB1 can save growth inhibition caused by miR-326. We also confirmed that the growth inhibition caused by miR-326 is associated with AKT pathway activation. Taken together, our results indicate that miR-326 could serve as a potential diagnostic biomarker and therapeutic option for GC in the near future.

Indexed as

Cell Cycle CheckpointsCell Line, TumorCell ProliferationDown-RegulationGene Expression Regulation, NeoplasticHumansMicroRNAsNuclear ProteinsProto-Oncogene MasProto-Oncogene Proteins c-aktRNA-Binding ProteinsStomach NeoplasmsMAS1 protein, humanMicroRNAsMIRN326 microRNA, humanNOB1 protein, humanNuclear ProteinsProto-Oncogene MasProto-Oncogene Proteins c-aktRNA-Binding Proteins

Identifiers

PMID27733214
PMCPMC7841105

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.