hMAGEA2 promotes progression of breast cancer by regulating Akt and Erk1/2 pathways
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Song Park1,*, Yonghun Sung1,*, Jain Jeong1, Minjee Choi1, Jinhee Lee1, Wookbong Kwon1, Soyoung Jang1, Si Jun Park1, Hyeng-Soo Kim1, Mee-Hyun Lee3, Dong Joon Kim3, Kangdong Liu3, Sung-Hyun Kim2,3, Zigang Dong3, Zae Young Ryoo1, Myoung Ok Kim4
1School of Life Science, BK21 Plus KNU Creative Bio Research Group, College of Natural Sciences, Kyungpook National University, Buk-ku, Daegu 41566, Republic of Korea
2Institute of Life Science and Biotechnology, Kyungpook National University, Buk-ku, Daegu 41566, Republic of Korea
3China-US(Henan) Hormel Cancer Institute, Zhengzhou, Henan 450008, China
4The School of Animal BT Science, Kyungpook National University, Sangju-si, Gyeongsangbuk-do 37224, Republic of Korea
*These authors contributed equally to this work
Myoung Ok Kim, email: [email protected]
Zae Young Ryoo, email: [email protected]
Keywords: hMAGEA2, breast cancer, triple-negative breast cancer, metastasis, Akt
Received: December 14, 2016 Accepted: March 06, 2017 Published: March 14, 2017
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.
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