Evidence map›Paper›PMID 33178684›Full record

ArticleFrontiers in cell and developmental biology2020

LncRNA AC010789.1 Promotes Colorectal Cancer Progression by Targeting MicroRNA-432-3p/ZEB1 Axis and the Wnt/β-Catenin Signaling Pathway.

Weili Duan, Xue Kong, Juan Li, Peilong Li, Yinghui Zhao, Tong Liu, Helen Barong Binang, Yunshan Wang, Lutao Du, Chuanxin Wang

Abstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

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  13. Long Non-coding RNAFrontiers in cell and developmental biology · 2020
    Article
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

10 authors.

Weili DuanDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xue KongDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Juan LiDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Peilong LiDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Yinghui ZhaoDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Tong LiuDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Helen Barong BinangDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Yunshan WangDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Lutao DuDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Chuanxin WangDepartment of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating literatures have indicated that long non-coding RNAs (lncRNAs) are crucial molecules in tumor progression in various human cancers, including colorectal cancer (CRC). However, the clinical significance and regulatory mechanism of a vast majority of lncRNAs in CRC remain to be determined. The current study aimed to explore the function and molecular mechanism of lncRNA AC010789.1 in CRC progression. AC010789.1 found to be overexpressed in CRC tissues and cells. High expression of AC010789.1 was associated with lymph node metastasis and poor prognosis. Moreover, AC010789.1 silencing inhibited proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro as well as tumorigenesis and metastasis in vivo. Mechanistically, we demonstrated that repression of AC010789.1 promoted miR-432-3p expression, and miR-432-3p directly binds to ZEB1. We then proved the anti-tumor role of miR-432-3p in CRC, showing that the inhibitory effect of AC010789.1 knockdown on CRC cells was achieved by the upregulation of miR-432-3p but downregulation of ZEB1. We also established that silencing AC010789.1 suppressed the Wnt/β-catenin signaling pathway. However, this inhibitory effect was partially counteracted by inhibition of miR-432-3p. In summary, these results reveal that silencing AC010789.1 suppresses CRC progression via miR-432-3p-mediated ZEB1 downregulation and suppression of the Wnt/β-catenin signaling pathway, highlighting a potentially promising strategy for CRC treatment.

Indexed as

AC010789.1colorectal cancerMicroRNA-432-3pprogressionZEB1

Identifiers

PMID33178684
PMCPMC7593606

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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.