Song Myung-Ha, Kim Ye-Rin, Bae Jae-Ho, Shin Dong-Hoon, Lee Sang-Yull
Department of Biochemistry, School of Medicine, Pusan National University, Yangsan, 626-870, Gyeongsangnam-do, Republic of Korea.
Department of Pathology, School of Medicine, Pusan National University, Yangsan, 626-870, Gyeongsangnam-do, Republic of Korea.
Biochem Biophys Res Commun. 2017 Mar 4;484(2):298-303. doi: 10.1016/j.bbrc.2017.01.105. Epub 2017 Jan 23.
The cancer/testis (CT) antigen NY-SAR-35 gene is located on the X chromosome and is aberrantly expressed in various cancers but not in normal tissues, other than testes. Previously, we reported the expression of NY-SAR-35 enhanced cell growth, proliferation, and invasion in HEK293 and cancer cells. To extend understanding of the NY-SAR-35 gene, we used a next generation sequencing (NGS) approach. NY-SAR-35 expression induced growth, proliferation, metastasis, and stemness genes, as indicated by the up-regulations of CXCR4, EpCAM, CD133, and CD44, at the mRNA and protein levels. The expression of NY-SAR-35 in HEK293 cells significantly increased ERK phosphorylation, but not the phosphorylation of AKT. In HEK293/NY-SAR-35 cells, the expressions of pro-apoptotic proteins, including p53, Bax, and p21, were reduced and that of cyclin E was increased. Also, NY-SAR-35 increased the expressions of pluripotency genes (Nanog, Oct-4, and Sox2) and the ability of HEK293 cells to form colonies. Taken together, the present study indicates NY-SAR-35 functions as a CT antigen that triggers oncogenesis and self-renewal.
癌/睾丸（CT）抗原NY-SAR-35基因位于X染色体上，在各种癌症中异常表达，但在除睾丸外的正常组织中不表达。此前，我们报道NY-SAR-35的表达增强了HEK293细胞和癌细胞的生长、增殖及侵袭能力。为了进一步了解NY-SAR-35基因，我们采用了下一代测序（NGS）方法。如CXCR4、EpCAM、CD133和CD44在mRNA和蛋白质水平的上调所示，NY-SAR-35的表达诱导了生长、增殖、转移和干性基因的表达。NY-SAR-35在HEK293细胞中的表达显著增加了ERK磷酸化，但未增加AKT磷酸化。在HEK293/NY-SAR-35细胞中，包括p53、Bax和p21在内的促凋亡蛋白表达降低，而细胞周期蛋白E表达增加。此外，NY-SAR-35增加了多能性基因（Nanog、Oct-4和Sox2）的表达以及HEK293细胞形成集落的能力。综上所述，本研究表明NY-SAR-35作为一种CT抗原发挥作用，触发肿瘤发生和自我更新。
