Evidence map›Paper›PMID 25582198›Full record

ArticleMolecular and cellular biology2015

Role of microRNA 30a targeting insulin receptor substrate 2 in colorectal tumorigenesis.

Qian Zhang, Qingchao Tang, Dandan Qin, Lei Yu, Rui Huang, Guixiang Lv, Zhaoxia Zou, Xiao-chen Jiang, Chendan Zou, Wei Liu and 6 more

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  5. MiR-30a suppresses metastasis of gastric adenocarcinoma via targeting FAPα.Cancer biomarkers : section A of Disease markers · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Qian ZhangDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Qingchao TangDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Dandan QinDepartment of Nephrology, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Lei YuDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Rui HuangDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Guixiang LvDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Zhaoxia ZouDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Xiao-chen JiangDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Chendan ZouDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Wei LiuDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Jing LuoDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Zhixun ZhaoDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Shan MuhammadDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Guiyu WangDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Ying-gang ChenDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Xishan WangDepartment of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China Colorectal Cancer Institute of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China wxshan1208@126.com.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are dysregulated in many types of malignant diseases, including colorectal cancer. miRNA 30a (miR-30a) is a member of the miR-30 family and has been implicated in many types of cancers. In this study, we determined the expression of miR-30a in human colon cancer tissues and cell lines. miR-30a was found to be significantly downregulated in both the tissues and cell lines. Furthermore, overexpression of miR-30a inhibited, while silencing of miR-30a promoted, cell proliferation, migration, and invasion in vitro. Consistently, stable overexpression of miR-30a suppressed the growth of colon cancer cell xenografts in vivo. Moreover, bioinformatic algorithms and luciferase reporter assays revealed that insulin receptor substrate 2 (IRS2) is a direct target of miR-30a. Further functional studies suggested that repression of IRS2 by miR-30a partially mediated the tumor suppressor effect of miR-30a. In addition, miR-30a inhibited constitutive phosphorylation of Akt by targeting IRS2. Additionally, clinicopathological analysis indicated that miR-30a has an inverse correlation with the staging in patients with colon cancer. Taken together, our study provides the first evidence that miR-30a suppressed colon cancer cell growth through inhibition of IRS2. Thus, miR-30a might serve as a promising therapeutic strategy for colon cancer treatment.

Indexed as

AnimalsCarcinogenesisCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticColorectal NeoplasmsDown-RegulationFemaleGenes, Tumor SuppressorHCT116 CellsHumansInsulin Receptor Substrate ProteinsMiceMice, Inbred BALB CMice, NudeInsulin Receptor Substrate ProteinsIRS2 protein, humanMicroRNAsProto-Oncogene Proteins c-akt

Identifiers

PMID25582198
PMCPMC4333091
OpenAlexW2024715737

What OpenQuestion holds

Textmetadata
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Registered trials

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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.