Evidence map›Paper›PMID 32157498›Full record

ArticleJournal of physiology and biochemistry2020

Long non-coding RNA OIP5-AS1 promotes pancreatic cancer cell growth through sponging miR-342-3p via AKT/ERK signaling pathway.

Xiangpeng Meng, Jia Ma, Baosheng Wang, Xin Wu, Zhen Liu

Abstract read
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In one paragraph

Article in Journal of physiology and biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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  10. The role of lncRNA OIP5-AS1 in cancer development and progression.Apoptosis : an international journal on programmed cell death · 2022
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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

5 authors at 2 institutions in 1 country.

Xiangpeng MengDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Jia MaDepartment of Gastrointestinal Endoscopy, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110032, People's Republic of China.
Baosheng WangDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Xin WuDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Zhen LiuDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China. docliuz3@sina.com.ORCID http://orcid.org/0000-0002-1436-1574
China Medical University · CNFourth Affiliated Hospital of China Medical University · CN

Funding

Department of Science and Technology of Liaoning Province No. CA19
6 · The paper itself

Abstract

Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1), a long non-coding RNA (lncRNA), has been reported to link with the progression of some cancers. However, its biological functions and underlying molecular mechanisms in pancreatic cancer are largely unknown. The aim of this study was to investigate the role of lncRNA OIP5-AS1 in pancreatic cancer. Quantitative real-time PCR analysis revealed that OIP5-AS1 is highly expressed in pancreatic cancer tissues versus adjacent non-tumor tissues. In vitro functional assays showed that downregulation of OIP5-AS1 or overexpression of miR-342-3p inhibited the proliferation, decreased Ki67 expression, and induced cell cycle arrest in pancreatic cancer cells. The expression of cyclinD1, CDK4, and CDK6 was decreased by knockdown of OIP5-AS1. Moreover, we found that OIP5-AS1 acted as a miR-342-3p sponge to suppress its expression and function. Dual-luciferase assay confirmed the interaction of OIP5-AS1 and miR-342-3p and verified anterior gradient 2 (AGR2) as a direct target of miR-342-3p. Results showed that depletion of miR-342-3p abolished the inhibitory effects of OIP5-AS1 knockdown on pancreatic cancer cell growth. The expression of Ki67, AGR2, cyclinD1, CDK4, CDK6, p-AKT, and p-ERK1/2 was reversed by silencing of miR-342-3p in pancreatic cancer cells with OIP5-AS1 knockdown. Further, knockdown of OIP5-AS1 suppressed tumor growth in a xenograft mouse model of pancreatic cancer. OIP5-AS1 induced pancreatic cancer progression via activation of AKT and ERK signaling pathways. Therefore, we demonstrate that OIP5-AS1 functions as oncogene in pancreatic cancer and its downregulation inhibits pancreatic cancer growth by sponging miR-342-3p via targeting AGR2 through inhibiting AKT/ERK signaling pathway.

Indexed as

Signal TransductionAdenocarcinomaAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMicroRNAsOncogene ProteinsPancreatic NeoplasmsRNA, Long Noncodinglong noncoding RNA OIP5, humanMicroRNAsMIRN342 microRNA, humanOncogene ProteinsRNA, Long NoncodingCell growthlncRNA OIP5-AS1miR-342-3pPancreatic cancer

Identifiers

PMID32157498
OpenAlexW3011608214

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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.