Abstract
BackgroundBreast cancer (BC) is the most common cancer and the fifth leading cause of cancer mortality with 685,000 deaths worldwide in 2020. Long non-coding RNAs (lncRNAs) are critical in BC carcinogenesis and progression. However, the functional roles and mechanisms of SLC16A1-AS1 in BC are unknown.MethodsThe expression profile of SLC16A1-AS1 in BC patients was investigated using data from The Cancer Genome Atlas (TCGA) database and checked in 80 BC patients, followed by analyzing the prognostic value of SLC16A1-AS1 in the 80 BC patients. The biological functions of SLC16A1-AS1 were further examined in vivo and in vitro after overexpression of SLC16A1-AS1 in BC cells. Possible binding sites between SLC16A1-AS1 and miR-552-5p were predicted by miRDB and those between miR-552-5p and Wnt inhibitory factor-1 (WIF1) were predicted by miRanda, which were confirmed using dual-luciferase reporter assay with mutation. Spearman correlation assay was applied to evaluate the association between genes. Rescue experiments were further applied to investigate the molecular mechanisms involved.ResultsLower SLC16A1-AS1 expression in BC tissues was related to poor prognosis of BC patients. Upregulation of SLC16A1-AS1 suppressed BC cell viability, colony formation, invasion, and migration in vitro and growth in vivo via sponging miR-552-5p to release WIF1.ConclusionSLC16A1-AS1 is a tumor suppressor in BC, and lower SLC16A1-AS1 expression is an indicator of poor prognosis in BC patients. SLC16A1-AS1 inhibits BC carcinogenesis and progression via the SLC16A1-AS1/miR-552-5p/WIF1 pathway. SLC16A1-AS1 represents a novel diagnostic, therapeutic, and prognostic target for BC management.
Highlights
Breast cancer (BC) is the most common cancer and the fifth leading cause of cancer mortality with 685,000 deaths worldwide in 2020
To investigate the potential participation of SLC16A1-AS1 in BC carcinogenesis and development, we first investigated the Long non-coding RNAs (lncRNAs) expression pattern based on public BC (BRCA) databases (TCGA dataset) by the online tool GEPIA, which showed a significantly lower SLC16A1-AS1 expression in tumor (T, n = 1,085) tissues than in normal (N, n = 291) tissues of BC (BRCA) patients (Figure 1A)
After the 80 BC patients were divided into SLC16A1-AS1 low-expression (n = 40) and SLC16A1-AS1 high-expression (n = 40) groups with the cutoff value of SLC16A1-AS1 median expression in BC tissues, the survival curves of the BC patients with SLC16A1-AS1 high-expression and SLC16A1-AS1 lowexpression levels were plotted by Kaplan–Meier analysis, which showed a poor prognosis in BC patients with lower SLC16A1-AS1 expression (Figure 1D)
Summary
Breast cancer (BC) is the most common cancer and the fifth leading cause of cancer mortality with 685,000 deaths worldwide in 2020. The functional roles and mechanisms of SLC16A1-AS1 in BC are unknown. Breast cancer (BC) is the most common malignancy in women worldwide. BC accounts for one in four cancer cases, ranking first for incidence in 159 of 185 countries in 2020 [1]. Despite the developments in BC diagnosis and treatments, the prognosis of BC patients is still unsatisfactory. BC is the fifth leading cause of cancer mortality with 685,000 deaths globally and accounts for one in six cancer deaths, ranking first for mortality in 110 of 185 countries in 2020 [1, 2]. A comprehensive understanding of the mechanisms involved in BC carcinogenesis and metastasis is crucial to improve the clinical outcomes of BC patients
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