Circ_0058124 Aggravates the Progression of Papillary Thyroid Carcinoma by Activating LMO4 Expression via Targeting miR-370-3p

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Abstract

Background

Thyroid cancer is the most common malignant tumor in the endocrine system. Papillary thyroid carcinoma (PTC) accounts for the vast majority of cases in this cancer. Recently, the vital role of circular RNA (circRNA) has been acknowledged in various cancers, and this study aimed to investigate the role of circ_0058124 and related mechanism of its action in PTC.

Materials and Methods

The expression of circ_0058124, miR-370-3p and LIM domain only ( LMO4) was detected by qRT-PCR in tissue samples (PTC tissues or normal tissues, n=20) and cell lines (non-cancer cell line, Nthy-ori 3–1, and PTC cell lines, IHH-4 and TPC-1). For functional analysis, cell proliferation was investigated using CCK-8 assay and colony formation assay. Cell migration and invasion were determined using transwell assay, and cell migration was also assessed by wound healing assay. Cell apoptosis was monitored by flow cytometry assay. For mechanism analysis, the interaction between miR-370-3p and circ_0058124 or LMO4 predicted by the bioinformatics analysis was validated by dual-luciferase reporter assay or RIP assay. The effect of circ_0058124 on tumor growth in vivo was identified by establishing the Xenograft model.

Results

The expression of circ_0058124 was enhanced in PTC tissues and cells. Circ_0058124 knockdown inhibited viability, colony formation, migration and invasion and promoted apoptosis of PTC cells. Besides, circ_0058124 knockdown also blocked tumor growth in vivo. miR-370-3p was a target of circ_0058124, and circ_0058124 regulated the expression of LMO4, a target of miR-370-3p, by targeting miR-370-3p. Rescue experiments presented that miR-370-3p inhibition reversed the inhibitory effects of circ_0058124 knockdown on PTC development, and LMO4 overexpression reversed the effect of miR-370-3p restoration on PTC development.

Conclusion

Circ_0058124 promoted the development of PTC by mediating the miR-370-3p/ LMO4 axis, and circ_0058124, functioned as an oncogene in PTC, might be used as a promising biomarker for PTC diagnosis and treatment.

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Most cited references 26

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CircRNA circRNA_102171 promotes papillary thyroid cancer progression through modulating CTNNBIP1-dependent activation of β-catenin pathway

Wen Bi, Jiayu Huang, Chunlei Nie … (2018)

Background As a type of recently discovered noncoding RNA, circular RNAs (circRNAs) exert pivot biological functions in diverse cancers. However, the role of circRNA_102171 in papillary thyroid cancer (PTC) has not been investigated. Our study was focused on the functional investigation toward circRNA_102171 in PTC progression. And we also aimed to reveal its potential molecular mechanism. Methods The expression pattern of circRNA_102171 was determined using quantitative polymerase chain reaction (qPCR) in PTC samples and cell lines. Cell proliferation was examined utilizing CCK8, colony formation and EdU incorporation assays. Apoptosis was analyzed by Annexin V/PI staining and FACS detection. Cell migration and invasion was measured using Transwell assay. Tumor growth in vivo was determined through a xenograft assay. RNA-pulldown, RNA-IP (RIP) and RNA-EMSA were used to analyze the interaction between circRNA_102171 and CTNNBIP1. Results CircRNA_102171 expression was upregulated in tumor tissues and cell lines. CircRNA_102171 silencing suppressed PTC cell proliferation, migration and invasion while promoting apoptosis. CircRNA_102171 knockdown inhibited PTC growth in vivo. CircRNA_102171 interacted with CTNNBIP1 to block its interaction with the β-catenin/TCF3/TCF4/LEF1 complex, leading to activation of Wnt/β-catenin pathway. Conclusions CircRNA_102171 overexpression promotes PTC progression through activating Wnt/β-catenin pathway in a CTNNBIP1-dependent way.

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The biological basis for microRNA target restriction to the 3' untranslated region in mammalian mRNAs

Shuo Gu, Lan Jin, Feijie Zhang … (2009)

MicroRNAs (miRNAs) interact with target sites located in 3' untranslated regions (3'UTR) of mRNAs to down-regulate their expression when the appropriate miRNA is bound to target mRNA. To establish the functional importance of target localization in the 3' UTR, we modified the stop codon to extend the coding region of the transgene reporter through the miRNA target sequence. As a result, the miRNAs lost their ability to inhibit translation but retained their ability to function as siRNAs in mammalian cells in culture and in vivo. The addition of rare but not optimal codons upstream of the extended opening reading frame (ORF) made the miRNA target more accessible and restored miRNA-induced translational knockdown. Taken together, these results suggest that active translation impedes miRNA-programmed RISC association with target mRNAs, and support a mechanistic explanation for the localization of most miRNA target sites in noncoding regions of mRNAs in mammals.

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Papillary thyroid carcinoma: an update.

Virginia A LiVolsi (2011)

The past two decades have seen numerous developments in the understanding of the origins and biology of papillary thyroid carcinoma. Advances in molecular biology, clinicopathologic studies of new entities, facility with fine-needle aspiration biopsy, and new radiologic imaging techniques have allowed for earlier diagnosis of these tumors. However, these advances have also caused controversies in cytologic and histopathologic diagnoses as well as therapy decisions. This paper will focus on several pathologic aspects of papillary carcinoma, which impact on its biology and prognosis.

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Author and article information

Journal

Journal ID (nlm-ta): Cancer Manag Res

Journal ID (iso-abbrev): Cancer Manag Res

Journal ID (publisher-id): cmar

Journal ID (pmc): cancmanres

Title: Cancer Management and Research

Publisher: Dove

ISSN (Electronic): 1179-1322

Publication date (Electronic): 01 October 2020

Publication date Collection: 2020

Volume: 12

Pages: 9459-9470

Affiliations

[1 ]Department of Otorhinolaryngology & Head and Neck Surgery, Tianjin Third Central Hospital , Tianjin, People’s Republic of China

[2 ]Department of Diagnostic and Therapeutic Ultrasonography, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy , Tianjin, People’s Republic of China

Author notes

Correspondence: Hailing Wang Department of Diagnostic and Therapeutic Ultrasonography, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy , North Ring Lake West Road, Heyuan District, Tianjin300060, People’s Republic of China Tel/Fax +86 022–23340123 Email mimohg@163.com

Article

Publisher ID: 271778

DOI: 10.2147/CMAR.S271778

PMC ID: 7534870

PubMed ID: 33061633

SO-VID: b9489f4b-d267-4795-a940-37c5b18bd826

License:

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

History

Date received : 11 July 2020

Date accepted : 26 August 2020

Page count

Figures: 7, References: 31, Pages: 12

Funding

Funded by: no funding;

There is no funding to report.

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Circ_0058124 Aggravates the Progression of Papillary Thyroid Carcinoma by Activating LMO4 Expression via Targeting miR-370-3p

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Abstract

Background

Materials and Methods

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Conclusion

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Karger: Oncology

Most cited references 26

CircRNA circRNA_102171 promotes papillary thyroid cancer progression through modulating CTNNBIP1-dependent activation of β-catenin pathway

The biological basis for microRNA target restriction to the 3' untranslated region in mammalian mRNAs

Papillary thyroid carcinoma: an update.

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