Evidence map›Paper›PMID 35476233›Full record

ArticleJournal of cancer research and clinical oncology2022

miR-144 inhibits the IGF1R-ERK1/2 signaling pathway via NUDCD1 to suppress the proliferation and metastasis of colorectal cancer cells: a study based on bioinformatics and in vitro and in vivo verification.

Bin Han, Ke Xu, Dan Feng, Yang Bai, Yangqi Liu, Yuanyuan Zhang, Liming Zhou

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 7 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

7 authors at 3 institutions in 1 country.

Bin Han *GCP Center/Institute of Drug Clinical Trials, Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Ke Xu *Department of Pharmacology, West China School of Preclinical and Forensic Medicine, Sichuan University, No. 17 Renmin South Road, Chengdu, 610041, Sichuan, China.
Dan FengDepartment of Pharmacy, Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Yang BaiDepartment of Pharmacology, West China School of Preclinical and Forensic Medicine, Sichuan University, No. 17 Renmin South Road, Chengdu, 610041, Sichuan, China.
Yangqi LiuDepartment of Pharmacology, West China School of Preclinical and Forensic Medicine, Sichuan University, No. 17 Renmin South Road, Chengdu, 610041, Sichuan, China.
Yuanyuan ZhangDepartment of Pharmacology, West China School of Preclinical and Forensic Medicine, Sichuan University, No. 17 Renmin South Road, Chengdu, 610041, Sichuan, China. sarahyyzhang@hotmail.com.
Liming ZhouGCP Center/Institute of Drug Clinical Trials, Affiliated Hospital of North Sichuan Medical College, Nanchong, China. zhoulm108@163.com.ORCID http://orcid.org/0000-0003-3156-627X
Sichuan University · CNAffiliated Hospital of North Sichuan Medical College · CNNorth Sichuan Medical University · CN

Funding

Affiliated Hospital of North Sichuan Medical College Plan Projects 2019ZD005Nanchong City and School Cooperation Project 18SXHZ0324Nanchong City and School Cooperation Project 20SXQT0101Nanchong City and School Cooperation Project NSMC20170447National Natural Science Foundation of China 819θ3660Sichuan Education Plan Project 18ZB0219Sichuan Science and Technology Plan Project 2019YJ0386
6 · The paper itself

Abstract

purposeColorectal cancer (CRC) is a severe health condition characterized by high mortalities. NudC domain containing 1 (NUDCD1) is abnormally upregulated in multiple tumors and is recognized as a cancer antigen. In CRC, NUDCD1 upregulation accelerates tumor progression by activating the IGF1R-ERK1/2 signaling pathway. Its specific regulatory mechanisms, however, remain unclear.

methodsIn the present study, we predicted the regulators of NUDCD1 and analyzed the expression profile of NUDCD1 in CRC tissues using the gene chip dataset. We also determined the regulation between miR-144, NUDCD1 and IGF1R-ERK1/2 signaling in vitro and in vivo. Then, the expression of miR-144 in CRC tissues was detected and its cell functions were verified in vitro.

resultsAs predicted by bioinformatics, we found that NUDCD1 is a predicted target of miR-144 and confirmed that miR-144 directly binds to NUDCD1. In vitro and in vivo, miR-144 was determined to specifically regulate NUDCD1 expression and as such, can reduce the activity of the IGF1R-ERK1/2 signaling pathway. Moreover, miR-144 was significantly downregulated in CRC tissues; its levels were significantly negatively correlated with CRC primary range and lymph node metastasis. Cell function studies verified that miR-144 acts as a tumor suppressor, because it significantly inhibits the proliferation, metastasis, and invasion of CRC cells as well as inducing cell cycle arrest and apoptosis.

conclusionsOur study demonstrates that miR-144 regulates IGF1R-ERK1/2 signaling via NUDCD1 to inhibit CRC cell proliferation and metastasis. The miR-144/NUDCD1/IGF1R-ERK1/2 signaling axis may be crucial in the progression of CRC.

Indexed as

Colorectal NeoplasmsMicroRNAsAntigens, NeoplasmCell Line, TumorCell MovementCell ProliferationComputational BiologyGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemReceptor, IGF Type 1Signal TransductionAntigens, NeoplasmIGF1R protein, humanMicroRNAsMIRN144 microRNA, humanNUDCD1 protein, humanReceptor, IGF Type 1Colorectal cancerIGF1R-ERK1/2 signalingmiR-144NUDCD1

Identifiers

PMID35476233
PMCPMC11801163
OpenAlexW4224923674

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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.