Evidence map›Paper›PMID 25285168›Full record

ArticleTheranostics2014

MiR-194 deregulation contributes to colorectal carcinogenesis via targeting AKT2 pathway.

Hui-Jun Zhao, Lin-Lin Ren, Zhen-Hua Wang, Tian-Tian Sun, Ya-Nan Yu, Ying-Chao Wang, Ting-Ting Yan, Weiping Zou, Jie He, Yaou Zhang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Theranostics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

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  18. Small non-coding RNA and colorectal cancer.Journal of cellular and molecular medicine · 2019
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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 4 institutions in 2 countries.

Hui-Jun Zhao1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
Lin-Lin Ren1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
Zhen-Hua Wang1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
Tian-Tian Sun1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
Ya-Nan Yu1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
Ying-Chao Wang1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
Ting-Ting Yan1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
Weiping Zou2. Department of Surgery, University of Michigan, Ann Arbor, MI 48109, USA.
Jie He3. Key Lab in Healthy Science and Technology; Division of Life Science; Graduate School at Shenzhen; Tsinghua University; Shenzhen, China.
Yaou Zhang3. Key Lab in Healthy Science and Technology; Division of Life Science; Graduate School at Shenzhen; Tsinghua University; Shenzhen, China.
Jie Hong1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
Jing-Yuan Fang1. State Key Laboratory for Oncogenes and Related Genes Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Diseases, 145 Middle Shandong Road, Shanghai 200001, China.
State Key Laboratory of Oncogene and Related Genes · CNUniversity Town of Shenzhen · CNRenji Hospital · CNUniversity of Michigan · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have increasingly linked microRNAs to colorectal cancer (CRC). MiR-194 has been reported deregulated in different tumor types, whereas the function of miR-194 in CRC largely remains unexplored. Here we investigated the biological effects, mechanisms and clinical significance of miR-194. Functional assay revealed that overexpression of miR-194 inhibited CRC cell viability and invasion in vitro and suppressed CRC xenograft tumor growth in vivo. Conversely, block of miR-194 in APC(Min/+) mice promoted tumor growth. Furthermore, miR-194 reduced the expression of AKT2 both in vitro and in vivo. Clinically, the expression of miR-194 gradually decreased from 20 normal colorectal mucosa (N-N) cases through 40 colorectal adenomas (CRA) cases and then to 40 CRC cases, and was negatively correlated with AKT2 and pAKT2 expression. Furthermore, expression of miR-194 in stool samples was gradually decreased from 20 healthy cases, 20 CRA cases, then to 28 CRC cases. Low expression of miR-194 in CRC tissues was associated with large tumor size (P=0.006), lymph node metastasis (P=0.012) and shorter survival (HR =2.349, 95% CI = 1.242 to 4.442; P=0.009). In conclusion, our data indicated that miR-194 acted as a tumor suppressor in the colorectal carcinogenesis via targeting PDK1/AKT2/XIAP pathway, and could be a significant diagnostic and prognostic biomarker for CRC.

Indexed as

AnimalsCarcinogenesisCell Line, TumorColorectal NeoplasmsDown-RegulationFemaleHeterograftsHumansMaleMiceMice, NudeMicroRNAsProto-Oncogene Proteins c-aktSignal TransductionMicroRNAsMIRN194 microRNA, humanMIRN194 microRNA, mouseProto-Oncogene Proteins c-aktAKT2 pathwaybiomarkercarcinogenesis.colorectal cancermiR-194

Identifiers

PMID25285168
PMCPMC4183997
OpenAlexW2153843107

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.