Evidence map›Paper›PMID 27904771›Full record

ArticleAmerican journal of cancer research2016

Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function.

Shuanzhu Cao, Yanzhou Wang, Jinquan Li, Mingliang Lv, Haitao Niu, Yong Tian

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 115 citations in OpenAlex.

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  8. Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024
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17 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

6 authors at 1 institution in 1 country.

Shuanzhu CaoDepartment of The Fourth Neurosurgery, Central Hospital Cangzhou City Cangzhou 061000, Hebei Province, China.
Yanzhou WangDepartment of The Fourth Neurosurgery, Central Hospital Cangzhou City Cangzhou 061000, Hebei Province, China.
Jinquan LiDepartment of Neurosurgery, Botou Hospital Cangzhou 061000, Hebei Province, China.
Mingliang LvDepartment of Neurosurgery, Botou Hospital Cangzhou 061000, Hebei Province, China.
Haitao NiuDepartment of The Fourth Neurosurgery, Central Hospital Cangzhou City Cangzhou 061000, Hebei Province, China.
Yong TianDepartment of The Fourth Neurosurgery, Central Hospital Cangzhou City Cangzhou 061000, Hebei Province, China.
Cangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA associated with metastasis, and is a favorable prognostic factor for lung cancer. Recent studies have shown that MALAT1 plays an important role in many malignancies. However, little is known about the role of MALAT1 in glioma. In this study, we determined the expression of MALAT1 and explored its prognostic value in glioma. Further, we investigated the regulatory mechanism of MALAT1 in glioma progression. Our results showed that the expression of MALAT1 was significantly decreased in glioma specimens than in noncancerous brain tissues. In addition, MALAT1 expression was significantly correlated with tumor size, WHO grade and Karnofsky Performance Status (KPS), and was an independent prognostic factor for survival of glioma patients. The gain- and loss-of-function experiments revealed miR-155 down-regulation by MALAT1, resulting in reciprocal effects. Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. The miR-155-induced tumorigenesis is mediated through FBXW7 function. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway. In conclusion, our data demonstrated that MALAT1 may be a novel prognostic biomarker and therapeutic target in glioma. Restoration of MALAT1 levels represents a novel therapeutic strategy against glioma.

Indexed as

cell viabilityFBXW7gliomaMALAT1miR-155

Identifiers

PMID27904771
PMCPMC5126273
OpenAlexW2560126974

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.