Bladder cancer (BC) is the most common genitourinary malignancy worldwide, and its aetiology and pathogenesis remain unclear. Accumulating evidence has shown that HAGLROS is closely related to the occurrence and progression of various cancers. However, the biological functions and underlying mechanisms of HAGLROS in BC remain unknown. In the present study, the expression of HAGLROS in BC was determined by public dataset analysis, transcriptome sequencing analysis, qRT-PCR and ISH assays. Gain- or loss-of-function assays were performed to study the biological roles of HAGLROS in BC cells and nude mouse xenograft model. Bioinformatic analysis, qRT-PCR, western blot, immunohistochemistry, FISH assays, subcellular fractionation assays and luciferase reporter assays were performed to explore the underlying molecular mechanisms of HAGLROS in BC. Here, we found that HAGLROS expression is significantly upregulated in BC tissues and cells, and elevated HAGLROS expression was related to higher pathologic grade and advanced clinical stage, which is significant for BC diagnosis. HAGLROS can enhance the growth and metastasis of BC and . Furthermore, miR-330-5p downregulation reversed the BC cells proliferation, migration and invasion inhibited by silencing HAGLROS. SPRR1B silencing restored the malignant phenotypes of BC cells promoted by miR-330--5p inhibitor. Mechanistically, we found that HAGLROS functions as a microRNA sponge to positively regulate SPRR1B expression by sponging miR-330-5p. Together, these results demonstrate that HAGLROS plays an oncogenic role and may serve as a potential biomarker for the diagnosis and treatment of BC.
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http://dx.doi.org/10.3389/fonc.2022.876090 | DOI Listing |
Curr Drug Targets
October 2024
Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, China.
HAGLR Opposite Strand lncRNA (HAGLROS) is a long non-coding RNA (lncRNA) located on the long arm of human chromosome 2 at locus 2q31.1. Emerging evidence highlights HAGLROS as a pivotal player in human cancers, characterized by its significant upregulation across multiple malignancies where it functions as an oncogenic driver.
View Article and Find Full Text PDFCell Death Dis
August 2024
Department of Central Laboratory, Yanbian University Hospital, Yanji, China.
Long non-coding RNAs (lncRNAs) play an important role in breast cancer progression, but the function of lncRNAs in regulating tumor-associated macrophages (TAMs) remains unclear. As carriers of lncRNAs, exosomes play an important role as mediators in the communication between cancer cells and the tumor microenvironment. In this study, we found that lncRNA HAGLROS was highly expressed in breast cancer tissues and plasma exosomes, and its high expression was related to the poor prognosis of breast cancer patients.
View Article and Find Full Text PDFAging (Albany NY)
December 2023
Chenzhou First People’s Hospital, Beihu, Chenzhou 423000, Hunan, China.
Objective: Papillary thyroid cancer (PTC) is one of the most serious diseases of the endocrine system. In view of the limited therapeutic effects of current medical methods, this study starts from the molecular level and looks for potential treatments. The interaction between HAGLROS/miR-206/HMGA2 was studied using multi-omics methods, which provided new ideas and methods for future treatments.
View Article and Find Full Text PDFOncol Rep
October 2023
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, Jiangsu 211166, P.R. China.
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that a pair of the wound‑healing assay data panels featured in Fig. 2E on p. 1011 (namely, the PLZF / 0 h and 48 h data panels for the BGC823 cell line) had also appeared in another article containing a majority of the same authors that had already been published [Chen J‑F, Wu P, Xia R, Yang J, Huo X‑Y, Gu D‑Y, Tang C‑J, We D and Yang F: STAT3‑induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal‑mediated inhibition of autophagy.
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