Evidence map›Paper›PMID 31217868›Full record

ArticleAmerican journal of translational research2019

miR-23a-5p inhibits cell proliferation and invasion in pancreatic ductal adenocarcinoma by suppressing ECM1 expression.

Wenjie Huang, Yaohuan Huang, Jianyou Gu, Junfeng Zhang, Jiali Yang, Songsong Liu, Chuanming Xie, Yingfang Fan, Huaizhi Wang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 23 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

9 authors at 2 institutions in 1 country.

Wenjie HuangDepartment of First Hepatobiliary Surgery, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, China.
Yaohuan HuangDepartment of First Hepatobiliary Surgery, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, China.
Jianyou GuDepartment of First Hepatobiliary Surgery, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, China.
Junfeng ZhangInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Army Medical University Chongqing 400038, China.
Jiali YangInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Army Medical University Chongqing 400038, China.
Songsong LiuInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Army Medical University Chongqing 400038, China.
Chuanming XieInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Army Medical University Chongqing 400038, China.
Yingfang FanDepartment of First Hepatobiliary Surgery, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, China.
Huaizhi WangInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Army Medical University Chongqing 400038, China.
Army Medical University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a genetic disease and a leading cause of cancer-related mortality. However, the molecular mechanism underlying PDAC progression remains unclear. In this study, we first confirmed that ECM1 is significantly upregulated in PDAC tissues and that its high levels of expression are closely associated with an advanced histologic grade and a poor prognosis using The Cancer Genome Atlas (TCGA) dataset and the Gene Expression Omnibus (GEO) database. We then found that miR-23a-5p binds directly to the ECM1 3'-untranslated region (3'-UTR), thereby inhibiting ECM1 expression. Functional studies revealed that the induced expression of ECM1 promoted oncogenic abilities and reversed the suppressive effects induced by miR-23a-5p. Collectively, our findings indicate that ECM1 is a proto-oncogene and show that targeting the miR-23a-5p/ECM1 axis may represent a promising therapeutic strategy for PDAC.

Indexed as

ECM1invasionmiR-23a-5ppancreatic ductal adenocarcinoma (PDAC)proliferation

Identifiers

PMID31217868
PMCPMC6556669
OpenAlexW2998350930

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.