目的：利用RNA干涉技术抑制雄激素受体（AR）的表达，研究AR在激素依赖性和激素非依赖性前列腺癌细胞增殖中的作用。
AIM: To study the role of androgen receptor (AR) in hormone-dependent and hormone-independent prostate cancer cell proliferation by knocking down AR expression with adenovirus-delivered siRNA.
按其介导的功能，可分为NK细胞激活性受体(NKAR)与NK细胞抑制性受体(NKIR)。
Based on function, NK cell receptors can be divided into activation receptors (NKAR) and inhibition receptors (NKIR).
NK细胞的活化受到活化性与抑制性受体的共同调控，由于识别机制的多样化，近年来，NK细胞表面活化性受体得到了人们的广泛关注。
The immune response of NK cell has been regulated by both activating receptors and inhibitory receptors which expressed on NK cell surface.
如这类反应是发生在雌激素依赖性肿瘤细胞内的雌激素受体上，可能会有抑制肿瘤生长的作用。
If these reactions occurred on the estrogen receptors in the cells of estrogen-dependent tumors, the growth of tumors may be inhibited.
如这类反应是发生在雌激素依赖性肿瘤细胞内的雌激素受体上，可能会有抑制肿瘤生长的作用。
If these reactions occurred on the estrogen receptors in the cells of estrogen-dependent tumors, the growth of tumors may be inhibited.
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