Evidence map›Paper›PMID 32355542›Full record

ArticleAmerican journal of translational research2020

ARNTL2 knockdown suppressed the invasion and migration of colon carcinoma: decreased SMOC2-EMT expression through inactivation of PI3K/AKT pathway.

Min Lu, Liyun Huang, Yinli Tang, Tao Sun, Jingyu Li, Sha Xiao, Xiangtao Zheng, Odong Christopher, Hua Mao

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-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

23 citing papers in PubMed, 31 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.

Min LuDepartment of Gastroenterology, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Liyun HuangDepartment of Gastroenterology, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Yinli TangDepartment of Gastroenterology, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Tao SunDepartment of Gastroenterology, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Jingyu LiDepartment of Pathology, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Sha XiaoDepartment of Pathology, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Xiangtao ZhengThe Second School of Clinical Medicine, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Odong ChristopherThe Second School of Clinical Medicine, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Hua MaoDepartment of Gastroenterology, Zhujiang Hospital, Southern Medical University Guangzhou 510280, Guangdong, P. R. China.
Zhujiang Hospital · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ARNTL2 is a transcriptional activator implicated in the molecular clock feedback system and is overexpressed in some malignant tumors. This study aimed to detect the effects of ARNTL2 knockdown by siRNA on the proliferation and invasion of colon carcinoma and clarify the molecular mechanisms of ARNTL2 in the development of colon carcinoma (CC). The CC microarray dataset GSE50760 was downloaded from the Gene Expression Omnibus (GEO) database. The expression levels of ARNTL2 in CC tissues and cancer cells were analyzed by immunohistochemistry and western blot, respectively. The knockdown of ARNTL2 expression was induced by RNA interference in colon cancer cells. The proliferation was detected by Cell Counting Kit-8 and clonal formation assays. The invasion and migration in vitro were detected by wound healing and transwell assays. Besides, a tumorigenicity test in the nude mice was performed to confirm whether ARNTL2 expression promoted the proliferation and invasion of CC cells. Furthermore, the expression of epithelial-mesenchymal transition (EMT) and PI3K/AKT signaling pathway-related factors were analyzed by western blot. Results showed that bioinformatics analysis found that ARNTL2 was upregulated in CC tissues. ARNTL2 was highly expressed in tissues and CC cells. Knockdown of ARNTL2 inhibited CC cells viability, colony formation, migration activity and reduced the size of tumors in the nude mice. Moreover, knockdown of ARNTL2 suppressed the expression of SMOC2, which may be the target gene of ARNTL2, and simultaneously inhibited the expression of EMT and PI3K/AKT signaling pathway-related factors. Taken together, downregulation of ARNTL2 could suppress CC cell proliferation and migration via SMOC2-EMT through inactivation of PI3K/AKT signaling pathway.

Indexed as

ARNTL2colon carcinomaepithelial mesenchymal transitionPI3K/Akt signaling pathwaySMOC2

Identifiers

PMID32355542
PMCPMC7191172
OpenAlexW3021016550

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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.