11月2日，日本东京大学的研究人员在美国《国家科学院学报》网络版上发表研究成果说，男性Y染色体上基因编码合成的一种蛋白质在睾丸细胞增殖过程中起到了“刹车”的作用，这种蛋白质或可延缓睾丸癌恶化进程。
此前的研究显示，雄性激素与其受体结合产生的某种物质如果过多进入睾丸细胞的细胞核，就会导致细胞异常增殖进而恶化。东京大学分子细胞生物学研究所教授加藤茂明等研究人员在研究中发现，男性Y染色体上基因合成的蛋白质“TSPY”能防止雄性激素与其受体结合产生的这种物质进入睾丸细胞的细胞核，而在睾丸癌恶化患者的细胞中，“TSPY”蛋白质的生成量不断减少。
研究人员还发现，睾丸癌恶化患者与没有恶化患者的Y染色体并不存在基因层面的差异，他们推测是在“TSPY”蛋白质的合成过程中发生了某种问题，才导致了上述结果。
睾丸癌多发生于性功能最活跃的20岁至40多岁的青壮年，如果恶化，转移到其他脏器的危险也很高。目前人们对睾丸癌的发病原因和恶化机制等知之甚少，除了切除睾丸外，睾丸癌还没有十分有效的治疗方法。（生物谷Bioon.com）
生物谷推荐英文摘要：
PNAS doi: 10.1073/pnas.1010307107
Testis-specific protein on Y chromosome (TSPY) represses the activity of the androgen receptor in androgen-dependent testicular germ-cell tumors
Chihiro Akimotoa, Takashi Uedaa,b, Kazuki Inouea, Ikuko Yamaokaa,c, Matomo Sakaria, Wataru Obarad, Tomoaki Fujiokad, Akira Nagaharae, Norio Nonomurae, Syuichi Tsutsumif, Hiroyuki Aburatanif, Tsuneharu Mikib, Takahiro Matsumotoa,c, Hirochika Kitagawaa,g, and Shigeaki Katoa,c,1
aThe Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan;
bDepartment of Urology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan;
cExploratory Research for Advanced Technology, Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan;
dDepartment of Urology, Iwate Medical University School of Medicine, Uchimaru, Morioka 020-5111, Japan;
eDepartment of Urology, Osaka University Graduate School of Medicine, Yamada-oka, Suita, Osaka 565-0871, Japan;
fGenome Science Division, Research Center for Advanced Science and Technology, University of Tokyo, Meguro-ku, Tokyo 153-8904, Japan; and
gInstitute for Molecular and Cellular Regulation, Gunma University, Showa-machi, Maebashi 371-8512, Japan
Testis-specific protein on Y chromosome (TSPY) is an ampliconic gene on the Y chromosome, and genetic interaction with gonadoblastoma has been clinically established. However, the function of the TSPY protein remains to be characterized in physiological and pathological settings. In the present study, we observed coexpression of TSPY and the androgen receptor (AR) in testicular germ-cell tumors (TGCTs) in patients as well as in model cell lines, but such coexpression was not seen in normal testis of humans or mice. TSPY was a repressor for androgen signaling because of its trapping of cytosolic AR even in the presence of androgen. Androgen treatment stimulated cell proliferation of a TGCT model cell line, and TSPY potently attenuated androgen-dependent cell growth. Together with the finding that TSPY expression is reduced in more malignant TGCTs in vivo, the present study suggests that TSPY serves as a repressor in androgen-induced tumor development in TGCTs and raises the possibility that TSPY could be used as a clinical marker to assess the malignancy of TGCTs.
