hMAGEA2 promotes progression of breast cancer by regulating Akt and Erk1/2 pathways

// Song Park 1, * , Yonghun Sung 1, * , Jain Jeong 1 , Minjee Choi 1 , Jinhee Lee 1 , Wookbong Kwon 1 , Soyoung Jang 1 , Si Jun Park 1 , Hyeng-Soo Kim 1 , Mee-Hyun Lee 3 , Dong Joon Kim 3 , Kangdong Liu 3 , Sung-Hyun Kim 2, 3 , Zigang Dong 3 , Zae Young Ryoo 1 , Myoung Ok Kim 4 1 School of Life Science, BK21 Plus KNU Creative Bio Research Group, College of Natural Sciences, Kyungpook National University, Buk-ku, Daegu 41566, Republic of Korea 2 Institute of Life Science and Biotechnology, Kyungpook National University, Buk-ku, Daegu 41566, Republic of Korea 3 China-US(Henan) Hormel Cancer Institute, Zhengzhou, Henan 450008, China 4 The School of Animal BT Science, Kyungpook National University, Sangju-si, Gyeongsangbuk-do 37224, Republic of Korea * These authors contributed equally to this work Correspondence to: Myoung Ok Kim, email: ok4325@knu.ac.kr Zae Young Ryoo, email: jaewoong64@hanmail.net Keywords: hMAGEA2, breast cancer, triple-negative breast cancer, metastasis, Akt Received: December 14, 2016      Accepted: March 06, 2017      Published: March 14, 2017 ABSTRACT Breast cancer is the most abundant cancer worldwide and a severe problem for women. Notably, breast cancer has a high mortality rate, mainly because of tumor progression and metastasis. Triple-negative breast cancer (TNBC) is highly progressive and lacks the expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Therefore, there are no established therapeutic targets against TNBC. In this study, we investigated whether the expression of human melanoma-associated antigen A2 (MAGEA2) is associated with TNBC. We found that hMAGEA2 is significantly overexpressed in human TNBC tissues; we also observed oncogenic properties using TNBC cell lines (MDA-MB-231 and MDA-MB-468). The overexpression of hMAGEA2 in MDA-MB-231 cell line showed dramatically increased cellular proliferation, colony formation, invasion, and xenograft tumor formation and growth. Conversely, knockdown of hMAEGA2 in MDA-MB-468 cell line suppressed cellular proliferation, colony formation, and xenograft tumor formation. Additionally, we showed that hMAGEA2 regulated the activation of Akt and Erk1/2 signaling pathways. These data indicate that hMAGEA2 is important for progression of TNBC and may serve as a novel molecular therapeutic target.