Knockdown of long non‐coding RNA LINC00176 suppresses ovarian cancer progression by BCL3‐mediated down‐regulation of ceruloplasmin

Autor: Jixiang Niu, Yanli Feng, Lan Dai
Rok vydání: 2019
Předmět:
Male
0301 basic medicine
B‐cell CLL/lymphoma 3
Mice
Nude
Apoptosis
Biology
medicine.disease_cause
Mice
03 medical and health sciences
0302 clinical medicine
Downregulation and upregulation
B-Cell Lymphoma 3 Protein
Cell Movement
Biomarkers
Tumor
Tumor Cells
Cultured
medicine
Animals
Humans
LINC00176
Epithelial–mesenchymal transition
RNA
Small Interfering
Cell Proliferation
Ovarian Neoplasms
Mice
Inbred BALB C
Reporter gene
Gene knockdown
epithelial‐mesenchymal transition
Ceruloplasmin
Original Articles
Cell Biology
Prognosis
medicine.disease
Xenograft Model Antitumor Assays
Long non-coding RNA
Gene Expression Regulation
Neoplastic
ovarian cancer
030104 developmental biology
030220 oncology & carcinogenesis
Cancer research
biology.protein
Molecular Medicine
Female
RNA
Long Noncoding
Original Article
Carcinogenesis
Ovarian cancer
Zdroj: Journal of Cellular and Molecular Medicine
ISSN: 1582-4934
1582-1838
Popis: Ovarian cancer is a common malignancy among women with some clinically approved diagnostic coding gene biomarkers. However, long non‐coding RNAs (lncRNAs) have been indicated to play an important role in controlling tumorigenesis of ovarian cancer. Hereby, the aim of the study was to uncover the function of lncRNA LINC00176 in the development and progression of ovarian cancer by regulating ceruloplasmin (CP). Bioinformatics prediction in combination with RT‐qPCR analysis for the expression pattern of LINC00176 revealed that LINC00176 was highly expressed in ovarian cancer tissues as well as in ovarian cancer cell lines, respectively. LINC00176 was predominantly localized in the nucleus. Delivery of si‐LINC00176, oe‐LINC00176, si‐BCL3 and si‐CP plasmids was conducted to explore the effects of LINC00176 on ovarian cancer. Promoted proliferation, migration and invasion along with reduced apoptosis were observed in cells treated with oe‐LINC00176, while si‐BCL3 and si‐CP were able to block the promoting effects. Investigations with regard to the correlation between LINC00176 and promoter region of CP turned out to be positive via B‐cell CLL/lymphoma 3 (BCL3) by means of dual‐luciferase reporter gene assay, ChIP and RIP assays. Furthermore, oncogenic properties of the LINC00176/BCL3/CP axis were also demonstrated by tumour formation in vivo generated upon injecting cells in nude mice. Our results demonstrate that restored LINC00176 initiates tumorigenesis in ovarian cancer by increasing CP expression via recruiting BCL3, the mechanism of which represented a potential and promising therapeutic target for the disease.
Databáze: OpenAIRE
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