11月2日，日本東京大學的研究人員在美國《國家科學院學報》網(wǎng)絡版上發(fā)表研究成果說,，男性Y染色體上基因編碼合成的一種蛋白質(zhì)在睪丸細胞增殖過程中起到了“剎車”的作用,，這種蛋白質(zhì)或可延緩睪丸癌惡化進程。
此前的研究顯示,，雄性激素與其受體結合產(chǎn)生的某種物質(zhì)如果過多進入睪丸細胞的細胞核,，就會導致細胞異常增殖進而惡化。東京大學分子細胞生物學研究所教授加藤茂明等研究人員在研究中發(fā)現(xiàn),，男性Y染色體上基因合成的蛋白質(zhì)“TSPY”能防止雄性激素與其受體結合產(chǎn)生的這種物質(zhì)進入睪丸細胞的細胞核,，而在睪丸癌惡化患者的細胞中，“TSPY”蛋白質(zhì)的生成量不斷減少,。
研究人員還發(fā)現(xiàn)，睪丸癌惡化患者與沒有惡化患者的Y染色體并不存在基因層面的差異,，他們推測是在“TSPY”蛋白質(zhì)的合成過程中發(fā)生了某種問題,，才導致了上述結果。
睪丸癌多發(fā)生于性功能最活躍的20歲至40多歲的青壯年,，如果惡化,，轉移到其他臟器的危險也很高。目前人們對睪丸癌的發(fā)病原因和惡化機制等知之甚少,，除了切除睪丸外,，睪丸癌還沒有十分有效的治療方法。（生物谷Bioon.com）
生物谷推薦英文摘要：
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.
