Evidence map›Paper›PMID 37667322›Full record

ArticleJournal of experimental & clinical cancer research : CR2023

Circadian gene ARNTL initiates circGUCY1A2 transcription to suppress non-small cell lung cancer progression via miR-200c-3p/PTEN signaling.

Deze Zhao, Yeping Dong, Minghao Duan, Dan He, Qun Xie, Wei Peng, Weifang Cui, Junjie Jiang, Yuanda Cheng, Heng Zhang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
6.0field-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

14 citing papers in PubMed, 39 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

14 authors at 3 institutions in 1 country.

Deze Zhao *Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yeping Dong *Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Minghao Duan *Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Dan HeHunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital & The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410008, Hunan, China.
Qun XieDepartment of Ultrasonic Imaging, Affiliated Hospital of Hunan Traditional Chinese Medicine Research Institute, Changsha, 410006, Hunan, China.
Wei PengDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Weifang CuiDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Junjie JiangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yuanda ChengDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Heng ZhangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Faqing TangHunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital & The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410008, Hunan, China.
Chunfang ZhangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yang GaoDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. gaoyang_george@sina.com.
Chaojun DuanDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. duancjxy@csu.edu.cn.
Central South University · CNXiangya Hospital Central South University · CNHunan Academy of Traditional Chinese Medicine · CN

Funding

Geriatric Research Education and Clinical Center 2021LNJJ17National Multidisciplinary Cooperative Diagnosis and Treatment Capacity Building Project for Major Diseases z027002National Natural Science Foundation of China 81572281National Natural Science Foundation of China 81702278National Natural Science Foundation of China 81974367National Natural Science Foundation of China 82003065National Natural Science Foundation of China 82172655Natural Science Foundation of Hunan Province 2023JJ30873Natural Science Foundation of Hunan Province 2020JJ4132Natural Science Foundation of Hunan Province 2021JJ70023Natural Science Foundation of Hunan Province 2022JJ30925
6 · The paper itself

Abstract

backgroundAs a subclass of endogenous stable noncoding RNAs, circular RNAs are beginning to be appreciated for their potential as tumor therapeutics. However, the functions and mechanisms by which circRNAs exert protective functions in non-small cell lung cancer (NSCLC) remain largely elusive.

methodsThe prognostic role of circGUCY1A2 was explored in lung adenocarcinoma specimens. The overexpressed and knockdown plasmids were used to evaluate the effect of circGUCY1A2 on NSCLC cell proliferation and apoptosis efficacy. Luciferase reporter system is used to prove that circGUCY1A2 could bind to miRNA. Chip-PCR was used to prove that circGUCY1A2 could be initiated by transcription factors ARNTL. Subcutaneous tumorigenicity grafts models were established to validate findings in vivo.

resultsThe expression of circGUCY1A2 were significantly reduced (P < 0.001) and negatively correlated with tumor size (P < 0.05) in non-small cell lung cancer (NSCLC). CircGUCY1A2 upregulation promoted apoptosis and inhibits cell proliferation and growth of subcutaneous tumorigenicity grafts in nude mice (P < 0.01). In addition, intra-tumor injection of pLCDH-circGUCY1A2 inhibited tumor growth in patient-derived NSCLC xenograft models (PDX). Mechanism studies showed that circGUCY1A2 could act as a sponge to competitively bind miR-200c-3p, promote PTEN expression, and thereby inhibit PI3K/AKT pathway. In addition, we found that the circadian gene ARNTL, which was reduced in NSCLC and prolonged the overall survival of patients, could bind to the promoter of circGUCY1A2, thereby increasing its expression.

conclusionsThis study is an original demonstration that ARNTL can inhibit the development of lung adenocarcinoma through the circGUCY1A2/miR-200c-3p/PTEN axis, and this finding provides potential targets and therapeutic approaches for the treatment of lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungARNTL Transcription FactorsCarcinoma, Non-Small-Cell LungLung NeoplasmsRNA, CircularAnimalsDisease Models, AnimalHumansMiceMice, NudePhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseSoluble Guanylyl CyclaseARNTL Transcription FactorsGUCY1A2 protein, humanPhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePTEN protein, humanRNA, CircularSoluble Guanylyl CyclaseARNTLcircGUCY1A2miR-200c-3pNon-small cell lung cancerPTEN

Identifiers

PMID37667322
PMCPMC10478228
OpenAlexW4386421869

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.