PT  - JOURNAL ARTICLE
AU  - ZIQIAN FANG
AU  - CHARLOTTE KILLICK
AU  - CERITH HALFPENNY
AU  - NATASHA FREWER
AU  - KATHRYN A. FREWER
AU  - FIONA RUGE
AU  - WEN G. JIANG
AU  - LIN YE
TI  - Sex Hormone-regulated <em>CMG2</em> Is Involved in Breast and Prostate Cancer Progression
AID  - 10.21873/cgp.20353
DP  - 2022 Nov 01
TA  - Cancer Genomics - Proteomics
PG  - 703--710
VI  - 19
IP  - 6
4099  - http://cgp.iiarjournals.org/content/19/6/703.short
4100  - http://cgp.iiarjournals.org/content/19/6/703.full
SO  - Cancer Genomics Proteomics2022 Nov 01; 19
AB  - Background/Aim: Capillary morphogenesis gene 2 (CMG2) is involved in prostate and breast cancer progression. This study aimed to investigate sex hormone receptor-mediated regulation of CMG2 in breast and prostate cancer, and its implication in disease progression. Materials and Methods: Expression of CMG2, oestrogen receptor (ER) and androgen receptor (AR) was determined in breast and prostate cancer cell lines, respectively, using real-time quantitative PCR (QPCR) and western blot. Association between CMG2 and sex hormone receptors was analysed in a number of transcriptome datasets. Immunochemical staining was performed in tissue microarrays of breast cancer (BR1505D) and prostate cancer (PR8011A). CMG2 expression was determined in 17β-oestradiol treated breast cancer cells and AR over-expressing prostate cancer cells. Results: CMG2 was found to be inversely correlated with sex hormone receptors in breast and prostate cancer. Lower expression of CMG2 was associated with a poor prognosis in ER (+) breast cancer but not ER (−) tumours. Both ER (+) breast cancer cell lines and AR (+) prostate cancer cell lines presented lower expression of CMG2, which was increased following sex hormone deprivation. Exposure to 17-β-oestradiol and AR over-expression repressed CMG2 expression in breast cancer and prostate cancer cell lines, respectively. Conclusion: CMG2 is inversely correlated with ER and AR status in breast and prostate cancer, respectively. ER and AR mediate repression of CMG2 expression in corresponding cancerous cells.