Abstract
Ovarian cancer affects >295,000 women worldwide and is the most lethal of gynaecological malignancies. Often diagnosed at a late stage, current research efforts seek to further the molecular understanding of its aetiopathogenesis and the development of novel biomarkers. The present study investigated the expression levels of the glucogenic hormone asprosin [encoded by fibrillin-1 (FBN1)], and its cognate receptor, olfactory receptor 4M1 (OR4M1), in ovarian cancer. A blend of in silico open access The Cancer Genome Atlas data, as well as in vitro reverse transcription-quantitative PCR (RT-qPCR), immunohistochemistry and immunofluorescence data were used. RT-qPCR revealed expression levels of OR4M1 and FBN1 in clinical samples and in ovarian cancer cell lines (SKOV-3, PEO1, PEO4 and MDAH-2774), as well as the normal human ovarian surface epithelial cell line (HOSEpiC). Immunohistochemical staining of a tissue microarray was used to identify the expression levels of OR4M1 and asprosin in ovarian cancer samples of varying histological subtype and grade, including clear cell carcinoma, serous ovarian cancer and mucinous adenocarcinoma. Immunofluorescence analysis revealed asprosin expression in SKOV-3 and HOSEpiC cells. These results demonstrated the expression of both asprosin and OR4M1 in normal and malignant human ovarian tissues. This research invokes further investigation to advance the understanding of the role of asprosin and OR4M1 within the ovarian tumour microenvironment.
Highlights
The tumour microenvironment has received growing interest owing to its role in metabolic dysregulation and tumorigenesis
We further analysed the co‐expression of FBN1 with the proteolytic enzyme furin, which may provide an oversight of potential furin‐mediated cleavage release of asprosin in these tissues (Fig. 1B)
This study presents novel data regarding the expression of FBN1, asprosin, and olfactory receptor 4M1 (OR4M1) in cancer, focusing on ovarian cancer
Summary
The tumour microenvironment has received growing interest owing to its role in metabolic dysregulation and tumorigenesis. Recent studies have associated dysregulation of extra cellular matrix (ECM) proteins, such as fibrillin‐1, with tumorigenesis. The structural glycoprotein, fibrillin‐1, is one of two cleavage. KERSLAKE et al: EXPRESSION LEVELS OF ASPROSIN AND OR4M1 IN OVARIAN CANCER products encoded by the FBN1 gene [1]. Cleavage produces the 320 kDa glycoprotein fibrillin‐1 and the recently discovered 30 kDa glucogenic hormone, asprosin [3]. The pathogenesis of NPS is attributed to premature ablation of profibrillin‐1 as a result of a truncation mutation within the FBN1 gene [3]. Investigation of NPS pathophysiology led to the classification of asprosin ‐ the c‐terminal cleavage product of profibrillin 1 ‐ as a novel orexigenic and glucogenic hormone, involved in the regulation of glucose homeostasis [3]
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