Evidence map›Paper›PMID 34991623›Full record

ArticleJournal of translational medicine2022

MiR-30c-5p loss-induced PELI1 accumulation regulates cell proliferation and migration via activating PI3K/AKT pathway in papillary thyroid carcinoma.

Tingting Zheng, Youxing Zhou, Xiaowei Xu, Xin Qi, Jiameng Liu, Yanan Pu, Shan Zhang, Xuerong Gao, Xinkai Luo, Mei Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

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  14. PELI1: key players in the oncogenic characteristics of pancreatic Cancer.Journal of experimental & clinical cancer research : CR · 2024
    Article
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  20. Ubiquitination Links DNA Damage and Repair Signaling to Cancer Metabolism.International journal of molecular sciences · 2023
    Review
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

14 authors at 4 institutions in 1 country.

Tingting Zheng *Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China.
Youxing ZhouDepartment of Surgery, Jiangyuan Hospital Affiliated To Jiangsu Institute of Nuclear Medicine, Wuxi, 214063, Jiangsu, People's Republic of China.
Xiaowei XuDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China.
Xin QiJiangsu Key Laboratory of Pathogen Biology, Department of Pathogen Biology and Immunology, Nanjing Medical University, Nanjing, 211166, Jiangsu, People's Republic of China.
Jiameng LiuDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China.
Yanan PuDepartment of Emergency Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, Jiangsu, People's Republic of China.
Shan ZhangDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China.
Xuerong GaoDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China.
Xinkai LuoDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China.
Mei LiDepartment of Pathology, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China.
Xuefeng WangDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China.
Liyang DongDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China. liyangdong@ujs.edu.cn.ORCID 0000-0002-2200-784X
Ying WangDepartment of Respiratory Diseases, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, 223002, Jiangsu, People's Republic of China. wangying_wyy@126.com.
Chaoming MaoDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, People's Republic of China. jq1001@ujs.edu.cn.
Jiangsu University · CNJiangsu Province Hospital · CNNanjing Medical University · CNXuzhou Medical College · CN

Funding

key research and development plan of Zhenjiang city SH2019047key research and development plan of Zhenjiang city SH2021050National Natural Science Foundation of China 81370889National Natural Science Foundation of China 81900562
6 · The paper itself

Abstract

backgroundThe aberrant expression of E3 ubiquitin ligase Pellino-1 (PELI1) contributes to several human cancer development and progression. However, its expression patterns and functional importance in papillary thyroid cancer (PTC) remains unknown.

methodsPELI1 expression profiles in PTC tissues were obtained and analyzed through the starBase v3.0 analysis. Real-time PCR, Immunohistochemical assays (IHC) and Western blot were used to investigate the mRNA and protein levels of PELI1 in PTC. The effects of PELI1 on PTC cell progression were evaluated through CCK-8, colony formation, Transwell, and Wound healing assay in vitro, and a PTC xenograft mouse model in vivo. The downstream target signal of PELI1 in PTC was analyzed by using Kyoto encyclopedia of genes and genomes (KEGG), and bioinformatics tools were used to identify potential miRNAs targeting PELI1. Human umbilical cord mesenchymal stem cells were modified by miR-30c-5p and the miR-30c-5p containing extracellular vesicles were collected (miR-30c-5p-EVs) by ultra-high-speed centrifugation method. Then, the effects of miR-30c-5p-EVs on PELI1 expression and PTC progression were evaluated both in vitro and in vivo.

resultsBoth mRNA and protein expression of PELI1 were widely increased in PTC tissues, and overexpression of PELI1 was positively correlated with bigger tumor size and lymph node metastases. PELI1 promoted PTC cell proliferation and migration in vitro. While, PELI1 silencing significantly suppressed PTC growth in vivo accompanied with reduced expression of Ki-67 and matrix metallopeptidase 2 (MMP-2). Mechanistically, PI3K-AKT pathway was identified as the downstream target of PELI1, and mediated the functional influence of PELI1 in PTC cells. Moreover, we found that the expression of miR-30c-5p was inversely correlated with PELI1 in PTC samples and further confirmed that miR-30c-5p was a tumor-suppressive miRNA that directly targeted PELI1 to inhibit PTC cell proliferation and migration. Furthermore, we showed that miR-30c-5p-EVs could effectively downregulate PELI1 expression and suppress the PTC cell growth in vitro and in vivo.

conclusionThis study not only supported the first evidence that miR-30c-5p loss-induced PELI1 accumulation facilitated cell proliferation and migration by activating the PI3K-AKT pathway in PTC but also provided novel insights into PTC therapy based on miR-carrying-hUCMSC-EVs.

Indexed as

Thyroid NeoplasmsAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMicroRNAsNuclear ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktThyroid Cancer, PapillaryUbiquitin-Protein LigasesMicroRNAsMIRN3113 microRNA, mouseNuclear ProteinsPELI1 protein, humanPeli1 protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktUbiquitin-Protein LigaseshUCMSC-EVsmiR-30c-5pPapillary thyroid carcinomaPELI1PI3K/AKT

Identifiers

PMID34991623
PMCPMC8740468
OpenAlexW4206401745

What OpenQuestion holds

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LicenceCC BY
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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.