RAB22A overexpression promotes the tumor growth of melanoma
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Feng Su1, Yifei Chen2, Shilin Zhu3, Fangfang Li4,5, Shuang Zhao4,5, Lisa Wu6, Xiang Chen4,5, Juan Su4,5
1Department of Emergency, Xiangya Hospital, Central South University, Changsha, China
2Department of Pharmacy, Xiangya Hospital, Central South University, Changsha, Hunan, China
3Department of Neurology, The Second Affiliated Hospital of Hunan University of TCM, Changsha, Hunan, China
4Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China
5Hunan Key Laboratory of Skin Cancer and Psoriasis, Xiangya Hospital, Central South University, Changsha, Hunan, China
6Institute of Medical Science Research, Xiangya Hospital, Central South University, Hunan, China
Juan Su, email: firstname.lastname@example.org
Keywords: melanoma, RAB22A, prognosis, malignant phenotype, microRNA
Received: July 25, 2016 Accepted: September 22, 2016 Published: September 28, 2016
Malignant melanoma is the most aggressive type of skin cancer. RAB22A, a member of RAS oncogene family, has been found to be significantly upregulated in multiple human cancers. In the present study, we found that RAB22A mRNA expression was significantly upregulated in melanoma tissues (including 60 primary melanomas and 84 metastatic melanomas) compared to benign nevi (n = 20), which were significantly higher in metastatic melanoma tissues than primary tissues. Immunohistochemistry data further showed that the positive immunoreactivity of RAB22A was detected in 66% (95/144) melanoma tissues, but not in benign nevi. Moreover, high expression of RAB22A was significantly associated with advanced clinical stage in melanoma. Furthermore, patients with high RAB22A expression had shorter overall survival compared those with low expression of RAB22A. In-vitro study showed that RAB22A was also upregulated in melanoma cell lines WM35, A375, WM451, and SK-MEL-1, when compared with the normal melanocyte HM cells. Knockdown of RAB22A significantly reduced the proliferation, migration and invasion of melanoma A375 cells, while overexpression of RAB22A significantly promoted these malignant phenotypes. In addition, RAB22A was found to be a target of miR-203, a tumor suppressive miRNA in melanoma. Besides, miR-203 was downregulated in melanoma tissues and cell lines, when compared with benign nevi and HM cells, respectively. Taken these findings together, our study could validate an oncogenic role of RAB22A in melanoma, suggesting that RAB22A may be a potential therapeutic target for melanoma.
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