CircRPPH1 accelerates the proliferation and migration of bladder cancer via enhancing the STAT3 signaling pathway

Bladder cancer (BCa) is a common malignant disease with high recurrence and variable prognosis. Circular RNAs (circRNAs) are implicated in the development of multiple diseases. However, the biological activities of circRNAs in BCa remain largely elusive. In the present study, it was found that circR...

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Veröffentlicht in:Oncology reports 2023-05, Vol.49 (5), p.1, Article 103
Hauptverfasser: Liu, Xiao, Tong, Yonghua, Huang, Qiu, He, Yu, Shang, Haojie, Chen, Zhiqiang, Tang, Kun
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container_issue 5
container_start_page 1
container_title Oncology reports
container_volume 49
creator Liu, Xiao
Tong, Yonghua
Huang, Qiu
He, Yu
Shang, Haojie
Chen, Zhiqiang
Tang, Kun
description Bladder cancer (BCa) is a common malignant disease with high recurrence and variable prognosis. Circular RNAs (circRNAs) are implicated in the development of multiple diseases. However, the biological activities of circRNAs in BCa remain largely elusive. In the present study, it was found that circRPPH1 was upregulated in BCa cell lines compared with normal urothelial cells. CircRPPH1 downregulation could inhibit the proliferation, migration and invasion of BCa cells and . Mechanistically, it was demonstrated that circRPPH1 can act as a sponge of miR‑296‑5P to upregulate STAT3, and interact with FUS to promote phosphorylated (p)‑STAT3 nuclear transport. Overall, circRPPH1 could promote BCa progression through sponging miR‑296‑5p to upregulate the expression of STAT3 and interacting with FUS to promote p‑STAT3 nuclear transport. CircRPPH1 was first identified to play a tumorigenic role in BCa, which could be an underlying therapeutic target.
doi_str_mv 10.3892/or.2023.8540
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Circular RNAs (circRNAs) are implicated in the development of multiple diseases. However, the biological activities of circRNAs in BCa remain largely elusive. In the present study, it was found that circRPPH1 was upregulated in BCa cell lines compared with normal urothelial cells. CircRPPH1 downregulation could inhibit the proliferation, migration and invasion of BCa cells and . Mechanistically, it was demonstrated that circRPPH1 can act as a sponge of miR‑296‑5P to upregulate STAT3, and interact with FUS to promote phosphorylated (p)‑STAT3 nuclear transport. Overall, circRPPH1 could promote BCa progression through sponging miR‑296‑5p to upregulate the expression of STAT3 and interacting with FUS to promote p‑STAT3 nuclear transport. 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Circular RNAs (circRNAs) are implicated in the development of multiple diseases. However, the biological activities of circRNAs in BCa remain largely elusive. In the present study, it was found that circRPPH1 was upregulated in BCa cell lines compared with normal urothelial cells. CircRPPH1 downregulation could inhibit the proliferation, migration and invasion of BCa cells and . Mechanistically, it was demonstrated that circRPPH1 can act as a sponge of miR‑296‑5P to upregulate STAT3, and interact with FUS to promote phosphorylated (p)‑STAT3 nuclear transport. Overall, circRPPH1 could promote BCa progression through sponging miR‑296‑5p to upregulate the expression of STAT3 and interacting with FUS to promote p‑STAT3 nuclear transport. 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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Bioinformatics
Biotechnology
Bladder cancer
Cancer therapies
Cell Line, Tumor
Cell Movement - genetics
Cell Proliferation - genetics
Cloning
Comparative analysis
Development and progression
Diseases
Gene Expression Regulation, Neoplastic
Health aspects
Humans
Kinases
Manufacturers
Manufacturing
Metastasis
MicroRNAs - genetics
Plasmids
Prognosis
Proteins
Relapse
RNA
RNA, Circular - genetics
Scientific equipment and supplies industry
Signal Transduction - genetics
Software
STAT3 Transcription Factor - genetics
STAT3 Transcription Factor - metabolism
Urinary Bladder Neoplasms - pathology
title CircRPPH1 accelerates the proliferation and migration of bladder cancer via enhancing the STAT3 signaling pathway
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