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A long non-coding RNA OLBC15 promotes triple-negative breast cancer progression via enhancing ZNF326 degradation.

ABSTRACT: BACKGROUND:The long non-coding RNAs (lncRNAs) have been involved in various processes, including cancer. However, the function of many lncRNAs is still elusive in triple-negative breast cancer (TNBC). METHODS:LncRNA profiling was used to screen for novel lncRNAs related to TNBC. OLBC15 expression was measured via qRT-PCR. In vitro migration and viability assays were conducted to determine the oncogenic role of OLBC15. Xenograft and metastatic models were performed to further investigate effects in vivo. RNA immunoprecipitation (RIP), mass spectrometry (MS), and fluorescence in situ hybridization (FISH) strategies were designed to identify the interaction between ZNF326 and OLBC15. RESULTS:In the current study, we have identified a novel oncogenic lncRNA termed OLBC15 via lncRNA profiling. OLBC15 is highly expressed especially in triple-negative breast cancer. OLBC15 promoted viability and migration in breast cancer cells. Moreover, OLBC15 could accelerate metastasis and xenograft tumor growth. Mechanistic study suggested that OLBC15 could bind a well-characterized tumor suppressor ZNF326 and OLBC15-ZNF326 interaction resulted in ZNF326 destabilization. OLBC15 induced proteasomal ZNF326 degradation through enhanced ubiquitination. OLBC15 and ZNF326 protein expression is also negatively correlated in clinical specimens. CONCLUSIONS:Collectively, OLBC15 may serve as an oncogenic lncRNA to facilitate TNBC progression and a putative target for therapeutic anti-breast cancer intervention.

SUBMITTER: Deng C

PROVIDER: S-EPMC7439339 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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A long non-coding RNA OLBC15 promotes triple-negative breast cancer progression via enhancing ZNF326 degradation.

Deng Chao C Zhang Bojuan B Zhang Yao Y Xu Xiaogang X Xiong Deming D Chen Xiaoyan X Wu Jiaojiao J

Journal of clinical laboratory analysis 20200424 8

<h4>Background</h4>The long non-coding RNAs (lncRNAs) have been involved in various processes, including cancer. However, the function of many lncRNAs is still elusive in triple-negative breast cancer (TNBC).<h4>Methods</h4>LncRNA profiling was used to screen for novel lncRNAs related to TNBC. OLBC15 expression was measured via qRT-PCR. In vitro migration and viability assays were conducted to determine the oncogenic role of OLBC15. Xenograft and metastatic models were performed to further inves ...[more]

PMID: 32329931

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Project description:Long non?coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) was reported to be a critical regulator of tumorigenesis and is frequently deregulated in several cancer types. However, the exact mechanism by which SNHG1 contributes to breast cancer progression has not been fully elucidated. The identification of the molecular mechanism of SNHG1 is important for understanding the development of breast cancer and for improving the prognosis of the patients with this disease. In the present study, increased expression levels of SNHG1 were noted in breast cancer tumors following analysis of differentially expressed lncRNAs between 1,063 tumor and 102 normal tissues derived from The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA?BRCA) dataset. This finding was further validated using 50 pairs of normal and tumor tissues that were collected from patients with breast cancer. Notably, SNHG1 expression was significantly correlated with estrogen receptor (ER)/progesterone receptor (PR) negative status (ER?/PR?) and advanced clinical stage in breast cancer tissues. Knockdown of SNHG1 led to cell growth arrest, cell cycle redistribution and cell migration inhibition of breast cancer cells. The miRDB database predicted that miR?573 interacts with SNHG1. RT?PCR confirmed the negative regulation of miR?573 levels by SNHG1 in breast cancer cells and the Dual?luciferase reporter assay confirmed their complementary binding. The repression of miR?573 by SNGH1 decreased LIM domain only 4 (LMO4) mRNA and protein expression levels in the breast cancer cell lines tested and induced the expression of cyclin D1 and cyclin E. In vitro experiments indicated that LMO4 overexpression could reverse siSNHG1?induced cell growth arrest, cell cycle redistribution and inhibition of cell migration in breast cancer cells. Moreover, the tumor xenograft model indicated that SNHG1 knockdown inhibited MDA?MB?231 growth in vivo and LMO4 overexpression reversed the tumor growth inhibition induced by SNHG1 knockdown. The present study demonstrated that SNHG1 acts as a novel oncogene in breast cancer via the SNHG/miR?573/LMO4 axis and that it could be a promising therapeutic target for patients with breast cancer.

Dataset Information

A long non-coding RNA OLBC15 promotes triple-negative breast cancer progression via enhancing ZNF326 degradation.

Publications

A long non-coding RNA OLBC15 promotes triple-negative breast cancer progression via enhancing ZNF326 degradation.

Similar Datasets

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