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

Song Park, Yonghun Sung, Jain Jeong, Minjee Choi, Jinhee Lee, Wookbong Kwon, Soyoung Jang, Si Jun Park, Hyeng Soo Kim, Mee Hyun Lee, Dong Joon Kim, Kangdong Liu, Sung Hyun Kim, Zigang Dong, Zae Young Ryoo, Myoung Ok Kim

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

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 melanomaassociated 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.

Original languageEnglish (US)
Pages (from-to)37115-37127
Number of pages13
JournalOncotarget
Volume8
Issue number23
DOIs
StatePublished - 2017

Bibliographical note

Funding Information:
This research was supported by Basic Science Research Program of the National Research Foundation of Korea (NRF), funded by the Ministry of Education (2014R1A6A3A04059193) and Science and Technology (No. 2014R1A1A2059813).

Publisher Copyright:
© Park et al.

Keywords

  • Akt
  • Breast cancer
  • Metastasis
  • Triple-negative breast cancer
  • hMAGEA2

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