Circular RNA dehydrodolichyl diphosphate synthase facilitated triple-negative breast cancer progression via miR-362-3p/DDX5 axis

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Suping Cui^1,2, Yong Zhang^1,2, Li Xing^1,2

¹Department of Pathology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.

Environmental Toxicology

|March 28, 2022

Abstract

Background:

Triple-negative breast cancer (TNBC) is a common hypotype of breast cancer. Circular RNAs (circRNAs) are burgeoning serve as vital controllers in numerous tumors. Nevertheless, the expression and regulatory mode of circRNAs in TNBC are still indistinct. This paper aimed to reveal the function and molecular mechanism of circular RNA dehydrodolichyl diphosphate synthase (circDHDDS) in TNBC.

Methods:

The contents of circDHDDS, DHDDS mRNA, microRNA-362-3p (miR-362-3p) and DEAD (Asp-Glu-Ala-Asp) box polypeptide 5 (DDX5) were indicated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. The colony formation assay and 5-ethynyl-2'-deoxyuridine (EdU) assay were executed to assess cell proliferation. The flow cytometry assay was utilized to detect cell apoptosis. The transwell assay and tube formation assay were applied to measure cell migration, invasion and angiogenesis. The targeted relationships of miR-362-3p and circDHDDS or DDX5 were forecasted and detected by dual-luciferase reporter assay. The in vivo test was implemented to confirm the effect of circDHDDS.

Results:

The contents of circDHDDS and DDX5 were increased, and miR-362-3p level was decreased in TNBC. CircDHDDS deficiency reserved cell proliferation, migration, invasion and angiogenesis, while facilitated cell apoptosis in TNBC cells. Furthermore, miR-362-3p was validated to exert a tumor repressive effect in TNBC cells by suppressing DDX5. Moreover, DDX5 could regulate the development of TNBC. The experimental data exposed that levels of miR-362-3p presented noteworthy negative correlation with circDHDDS and DDX5, while circDHDDS and DDX5 exhibited significant positive correlation. In mechanism, circDHDDS bound to miR-362-3p to modulate DDX5 expression. In addition, circDHDDS knock-down also attenuated tumor growth.

Conclusion:

CircDHDDS expedited TNBC by swelling DDX5 via adapting miR-362-3p.

Insights

Circular RNA dehydrodolichyl diphosphate synthase (circDHDDS) promotes triple-negative breast cancer (TNBC) by increasing DEAD box polypeptide 5 (DDX5) via sponging microRNA-362-3p. CircDHDDS deficiency inhibits TNBC cell proliferation, migration, invasion, and angiogenesis while promoting apoptosis.

Area of Science:

Molecular Oncology
Cancer Biology
Epigenetics

Background:

Triple-negative breast cancer (TNBC) is an aggressive subtype with limited therapeutic targets.
Circular RNAs (circRNAs) are emerging as critical regulators in cancer, but their roles in TNBC are not fully understood.
This study investigates the function and mechanism of circRNA dehydrodolichyl diphosphate synthase (circDHDDS) in TNBC pathogenesis.

Purpose of the Study:

To elucidate the role and molecular mechanism of circDHDDS in triple-negative breast cancer.
To determine the regulatory relationship between circDHDDS, microRNA-362-3p (miR-362-3p), and DEAD box polypeptide 5 (DDX5) in TNBC.

Main Methods:

Quantitative real-time PCR and western blot were used to measure expression levels of circDHDDS, DDX5, and miR-362-3p.
Cellular assays including colony formation, EdU, flow cytometry, transwell, and tube formation assays assessed proliferation, apoptosis, migration, invasion, and angiogenesis.
Dual-luciferase reporter assays and in vivo experiments validated the molecular interactions and functional effects of circDHDDS.

Main Results:

CircDHDDS and DDX5 expression were upregulated, while miR-362-3p was downregulated in TNBC tissues and cells.
CircDHDDS knockdown suppressed TNBC cell proliferation, migration, invasion, and angiogenesis, and induced apoptosis.
CircDHDDS acts as a molecular sponge for miR-362-3p, thereby increasing DDX5 expression, which promotes TNBC development.

Conclusions:

CircDHDDS significantly promotes TNBC progression by upregulating DDX5 expression through the sponging of miR-362-3p.
CircDHDDS represents a potential therapeutic target for triple-negative breast cancer.
The circDHDDS/miR-362-3p/DDX5 axis plays a crucial role in TNBC tumorigenesis.

Read full analysis

Keywords:

DDX5 circDHDDS miR-362-3p triple-negative breast cancer

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