Evidence map›Paper›PMID 23353818›Full record

ArticleOncogene2014

MicroRNA-296-5p increases proliferation in gastric cancer through repression of Caudal-related homeobox 1.

T Li, Y Y Lu, X D Zhao, H Q Guo, C H Liu, H Li, L Zhou, Y N Han, K C Wu, Y Z Nie and 2 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 104 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

12 authors at 2 institutions in 1 country.

T LiState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Y Y LuState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
X D ZhaoState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
H Q GuoState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
C H LiuState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
H LiState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
L ZhouState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Y N HanState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
K C WuState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Y Z NieState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Y Q ShiState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
D M FanState Key Laboratory of Cancer Biology and Department of Gastroenterology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Xijing Hospital · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caudal-related homeobox 1 (CDX1), an intestinal-specific transcription factor, has been reported to have vital roles in gastric intestinal metaplasia (IM). Although IM is a high-risk factor for gastric cancer (GC), the specific role of CDX1 in GC is largely unknown. In this study, we investigated the expression of CDX1 and its functional roles in GC, and its upstream regulatory mechanisms at the microRNA (miRNA) level were further explored. We found that CDX1 is lost in GC when compared with adjacent IM tissues. Gain-of-function studies showed that CDX1 significantly inhibited GC cell growth by inducing cell cycle arrest and apoptosis. Interestingly, we identified and verified an onco-mir, miR-296-5p, as a direct upstream regulator of CDX1. miR-296-5p overexpression significantly promoted GC cell growth and attenuated the CDX1-induced anti-growth effects by recurring cell cycle distribution and apoptotic status, whereas knockdown of miR-296-5p decreased GC cell growth. Furthermore, we found that the extracellular signal-regulated kinases 1 and 2 (ERK1/2) activation and the subsequent downstream changes in protein levels related to cell cycle and apoptosis partly account for the miR-296-5p-CDX1-induced GC growth promotion. In addition, the detection of miR-296-5p and expression of CDX1 in primary GC tissues and adjacent IM tissues revealed that miR-296-5p is inversely correlated with CDX1, further supporting our in vitro results. Our results showed an anti-growth effect of CDX1 and identified its miRNA regulatory mechanism in GC. The identification of this novel miR-296-5p-CDX1-ERK1/2 axis sheds new light on the understanding of the process from IM to GC and may provide therapeutic targets for the treatment of GC.

Indexed as

ApoptosisCell Growth ProcessesDown-RegulationGene Knockdown TechniquesGenes, HomeoboxHomeodomain ProteinsHumansMicroRNAsStomach NeoplasmsTransfectionCDX1 protein, humanHomeodomain ProteinsMicroRNAsMIRN296 microRNA, human

Identifiers

PMID23353818
OpenAlexW2046600573

What OpenQuestion holds

Textmetadata
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.