Evidence map›Paper›PMID 29520106›Full record

ArticleOncogene2018

microRNA-200a downregulation in human glioma leads to Gαi1 over-expression, Akt activation, and cell proliferation.

Yuan-Yuan Liu, Min-Bin Chen, Long Cheng, Zhi-Qing Zhang, Zheng-Quan Yu, Qin Jiang, Gang Chen, Cong Cao

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
4.6field-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

80 citing papers in PubMed, 110 citations in OpenAlex.

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20 more citing papers are in PubMed but not listed here.

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 5 institutions in 1 country.

Yuan-Yuan LiuClinical Research and Lab Center, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.
Min-Bin ChenDepartment of Radiotherapy and Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.
Long ChengJiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, China.
Zhi-Qing ZhangJiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, China.
Zheng-Quan YuDepartment of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Qin JiangThe Affiliated Eye Hospital of Nanjing Medical University, Nanjing, China. Jqin710@vip.sina.com.
Gang ChenDepartment of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China. nju_neurosurgery@163.com.
Cong CaoJiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, China. caocong@suda.edu.cn.
First Affiliated Hospital of Soochow University · CNFirst People's Hospital of Kunshan · CNSecond Affiliated Hospital of Nanjing Medical University · CNSecond Affiliated Hospital of Soochow University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously identified a pivotal role for G protein α inhibitory subunit 1 (Gαi1) in mediating PI3K-Akt signaling by receptor tyrosine kinases (RTKs). Here, we examined the expression and biological function of Gαi1 in human glioma. Gαi1 mRNA and protein expression were significantly upregulated in human glioma tissues, which correlated with downregulation of an anti-Gαi1 miRNA: microRNA-200a ("miR-200a"). Forced-expression of miR-200a in established (A172/U251MG lines) and primary (patient-derived) human glioma cells resulted in Gαi1 downregulation, Akt inactivation and proliferation inhibition. Reduction of Gαi1 expression by shRNA, dominant negative mutant interference, or complete Gαi1 depletion inhibited Akt activation and cell proliferation. Notably, miR-200a was unable to inhibit glioma cell proliferation when Gαi1 was silenced or mutated. Co-immunoprecipitation studies, in human glioma cells and tissues, show that Gαi1 forms a complex with multiple RTKs (EGFR, PDGFRα, and FGFR) and the adapter protein Gab1. In vivo, the growth of subcutaneous and orthotopic glioma xenografts in nude mice was largely inhibited by expression of Gαi1 shRNA or miRNA-200a. Collectively, miR-200a downregulation in human glioma leads to Gαi1 over-expression, Akt activation and glioma cell proliferation.

Indexed as

Down-RegulationAnimalsBrain NeoplasmsCell ProliferationGene Expression Regulation, NeoplasticGliomaGTP-Binding Protein alpha Subunits, Gi-GoHumansMiceMicroRNAsNeoplasm TransplantationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTumor Cells, CulturedGNAI1 protein, humanGTP-Binding Protein alpha Subunits, Gi-GoMicroRNAsMIRN200 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID29520106
OpenAlexW2790789557

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.