Abstract
BackgroundRecently, the roles of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in human diseases have been unveiled, this research was conducted to explore the impacts of lncRNA SET-binding factor 2-antisense RNA1 (SBF2-AS1), miR-143 and resistance to ralstonia solanacearum 1 (RRS1) on breast cancer (BC) development.MethodsThe expression of SBF2-AS1, miR-143 and RRS1 in BC tissues, as well as in MDA-MB-231 and MCF-7 cell lines were assessed. Subsequently, the cells were transfected with miR-143 mimics or/and silenced or overexpressed SBF2-AS1 plasmids, and their negative controls. Then the proliferation, colony formation ability, cell cycle arrest, apoptosis, invasion and migration of the cells were assessed through gain- and loss-of-function experiments. Furthermore, the tumor growth, ki-67 expression and apoptosis in vivo were observed by subcutaneous tumorigenesis in nude mice. Binding relation between SBF2-AS1 and miR-143, and that between miR-143 and RRS1 were confirmed.ResultsSBF2-AS1 and RRS1 were amplified, while miR-143 was reduced in BC tissues and cells. Reduced SBF2-AS1 and elevated miR-143 could repress the proliferation, invasion and migration via restraining RRS1 expression. Moreover, knockdown of SBF2-AS1 up-regulated miR-143 to promote the apoptosis of BC cells by downregulating RRS1, resulting in a prohibitive effect on the tumorigenesis and progression of BC. Results of in vivo experiments indicated that the inhibited SBF2-AS1 and overexpressed miR-143 could restrict BC cell proliferation and promote apoptosis, and decelerate tumor growth in xenografts.ConclusionWe have discovered in this study that down-regulated SBF2-AS1 could inhibit tumorigenesis and progression of BC by up-regulation miR-143 and repressing RRS1, which provides basic therapeutic considerations for a novel target against BC.
Highlights
The roles of long non-coding RNAs and microRNAs in human diseases have been unveiled, this research was conducted to explore the impacts of lncRNA SET-binding factor 2-antisense RNA1 (SBF2-AS1), miR-143 and resistance to ralstonia solanacearum 1 (RRS1) on breast cancer (BC) development
We studied whether lncRNA SBF2-AS1 could be a novel target for BC treatment, thereby helping to find efficient therapeutic strategies for BC, and we deduced that SET-binding factor 2-antisense RNA1 (SBF2AS1) could serve as a Competing endogenous RNA (ceRNA) to modulate the tumorigenesis and progression of BC by regulating miR-143 and RRS1
SBF2-AS1 and RRS1 are highly expressed, and miR-143 is poorly expressed in BC tissues The expression of SBF2-AS1, RRS1 and miR-143 in BC tissues and adjacent normal tissues was assessed by Reverse transcription quantitative polymerase chain reaction (RTqPCR), the results (Fig. 1a) reflected that relative to the adjacent normal tissues, the mRNA expression of SBF2AS1 and RRS1 was elevated, and miR-143 expression was repressed in the BC tissues
Summary
The roles of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in human diseases have been unveiled, this research was conducted to explore the impacts of lncRNA SET-binding factor 2-antisense RNA1 (SBF2-AS1), miR-143 and resistance to ralstonia solanacearum 1 (RRS1) on breast cancer (BC) development. The mortality of BC has been reduced in recent years in most high-income countries owing to the developed therapy and earlier diagnosis. The factors including gender, age, obesity, alcohol consumption, oral contraceptive, hormone replacement treatment, hereditary tendency and family history are all demonstrated to be implicated in the BC tumorigenesis [3]. Some clinicopathological parameters including histological type, histological grade, lymph node metastasis (LNM), and clinical stages have been generally applied in the management of BC, yet some patients with the same clinicopathological features have distinct prognosis [4]. In order to promote the therapeutic efficiency and prognosis of BC, critical mechanisms that modulate the tumor growth and progression of BC are sorely needed
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Journal of Experimental & Clinical Cancer Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.