Altered Expression of <i>ESR1</i>, <i>ESR2</i>, <i>PELP1</i> and <i>c-SRC</i> Genes Is Associated with Ovarian Cancer Manifestation

• Main Authors: Monika Englert-Golon, Mirosław Andrusiewicz, Aleksandra Żbikowska, Małgorzata Chmielewska, Stefan Sajdak, Małgorzata Kotwicka
• Format: Article
• Language: English
• Published: MDPI AG 2021-06-01
• Series: International Journal of Molecular Sciences
• Subjects: ovarian cancer; estrogen receptors (ESR1 and ESR2); proline-, glutamic acid-, and leucine-rich protein 1 (PELP1); proto-oncogene tyrosine-protein kinase c-Src (SRC); estrogen signal transduction coregulators
• Online Access: https://www.mdpi.com/1422-0067/22/12/6216

Ovarian cancer remains the leading cause of death due to gynecologic malignancy. Estrogen-related pathways genes, such as estrogen receptors (ESR1 and ESR2) and their coregulators, proline-, glutamic acid-, and leucine-rich protein 1 (PELP1), and proto-oncogene tyrosine-protein kinase c-Src (SRC) are involved in ovarian cancer induction and development, still they require in-depth study. In our study, tissue samples were obtained from 52 females of Caucasian descent (control group without cancerous evidence (<i>n</i> = 27), including noncancerous benign changes (<i>n</i> = 15), and the ovarian carcinoma (<i>n</i> = 25)). Using quantitative analyses, we investigated ESRs, PELP1, and SRC mRNA expression association with ovarian tumorigenesis. Proteins’ presence and their location were determined by Western blot and immunohistochemistry. Results showed that <i>PELP1</i> and <i>SRC</i> expression levels were found to differ in tissues of different sample types. The expression patterns were complex and differed in the case of ovarian cancer patients compared to controls. The most robust protein immunoreactivity was observed for PELP1 and the weakest for ESR1. The expression patterns of analyzed genes represent a potentially interesting target in ovarian cancer biology, especially PELP1. This study suggests that specific estrogen-mediated functions in the ovary and ovary-derived cancer might result from different local interactions of estrogen with their receptors and coregulators.