Evidence map›Paper›PMID 31372165›Full record

ArticleCellular & molecular biology letters2019

Long non-coding RNA Malat1 activated autophagy, hence promoting cell proliferation and inhibiting apoptosis by sponging miR-101 in colorectal cancer.

Yaoran Si, Zhaoguo Yang, Quanxing Ge, Lingbing Yu, Meiying Yao, Xinfang Sun, Zheng Ren, Chunsheng Ding

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular biology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.2field-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

59 citing papers in PubMed, 97 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

8 authors at 1 institution in 1 country.

Yaoran Si1Department of Gastroenterology, Huaihe Hospital, Henan University, Kaifeng, 475000 Henan China.
Zhaoguo YangDepartment of General Surgery, Kaifeng Central Hospital, Kaifeng, Henan China.
Quanxing Ge1Department of Gastroenterology, Huaihe Hospital, Henan University, Kaifeng, 475000 Henan China.
Lingbing Yu1Department of Gastroenterology, Huaihe Hospital, Henan University, Kaifeng, 475000 Henan China.
Meiying Yao1Department of Gastroenterology, Huaihe Hospital, Henan University, Kaifeng, 475000 Henan China.
Xinfang Sun1Department of Gastroenterology, Huaihe Hospital, Henan University, Kaifeng, 475000 Henan China.
Zheng Ren1Department of Gastroenterology, Huaihe Hospital, Henan University, Kaifeng, 475000 Henan China.
Chunsheng Ding1Department of Gastroenterology, Huaihe Hospital, Henan University, Kaifeng, 475000 Henan China.
Henan University Huaihe Hospital and Huaihe Clinical Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNA Malat1 has been widely identified as an oncogene which shows a significant relationship with tumorigenesis in colorectal cancer (CRC). Nonetheless, whether Malat1 participates in the autophagy of colorectal cancer remains unclear. MATERIALS AND

methodsFirst, the expression level of Malat1 in 96 pairs of colorectal cancer tissues and four cell lines was detected by qRT-PCR. Subsequently, the autophagy activity in colorectal cancer tissues and cell lines was detected by western blot. Furthermore, the CCK-8 assay and flow cytometry (FCM) were performed to detect the role of autophagy activated by Malat1 in colorectal cancer cell lines.

resultsIn this study, significantly increased Malat1 expression and autophagy activity were found in colorectal cancer tissues compared with the adjacent normal tissues. Also, the Malat1 level was positively correlated with the expression of LC3-II mRNA in vivo. Moreover, autophagy activation and cell proliferation were significantly facilitated by Malat1 in colorectal cancer cells, while apoptosis decreased. Above all, the inhibition of autophagy by 3-MA not only relieved the Malat1-induced cell proliferation but also promoted the Malat1-induced cell apoptosis. In addition, Malat1 was found to act as an endogenous sponge by directly binding to miR-101 to reduce miR-101. Furthermore, the suppressive effects of miR-101 on the autophagy, proliferation, and apoptosis of CRC were abolished by Malat1.

conclusionLong non-coding RNA Malat1 activated autophagy and promoted cell proliferation, yet inhibited apoptosis by sponging miR-101 in colorectal cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisAutophagyCell Line, TumorCell ProliferationColorectal NeoplasmsHumansMicroRNAsRNA, Long NoncodingMALAT1 long non-coding RNA, humanMicroRNAsMIRN101 microRNA, humanRNA, Long NoncodingApoptosisAutophagyColorectal cancerLong noncoding RNA Malat1miR-101Proliferation

Identifiers

PMID31372165
PMCPMC6660674
OpenAlexW2964359355

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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.