生长蛋白有望成为前列腺癌治疗的新靶点

yuji8

Growth Protein May Provide New Target for Prostate Cancer
NEW YORK (Reuters Health) Mar 20 - Inhibition of the signal transducer and activator of transcription 5a/b (Stat5a/b), the key mediator of prolactin effects in prostate cancer cells, kills cancer cells and inhibits xenograft growth in mice, researchers report in the March 1st issue of Clinical Cancer Research.
研究人员在3月份《临床癌症研究》第1期中报道抑制信号转导子和转录活化子5a/b（Stat5a/b）（即前列腺癌细胞中的催乳素效应的关键介导子）可以杀伤小鼠体内的癌细胞，抑制异种移植生长。

\"Identification of Stat5a/b as a therapeutic target protein for prostate cancer may eventually lead to new therapies...based on Stat5 inhibition,\" senior investigator Dr. Marja T. Nevalainen told Reuters Health.
资深研究者Dr. Marja T. Nevalainen说：“Stat5a/b的识别作为前列腺癌的异种治疗靶蛋白有望最终获得基于抑制Stat5的新型治疗方法。”

Dr. Nevalainen of Thomas Jefferson University, Philadelphia and colleagues explain that prolactin protein expression and activation of Stat5a/b are associated with a high histologic grade of clinical prostate cancer, and activation of Stat5a/b in primary prostate cancer predicts early disease recurrence.
费城Thomas Jefferson大学的Dr. Nevalainen和其同事们解释道，催乳素蛋白的表达和Stat5a/b的活化是与临床前列腺癌的高组织学分化相关的，初发前列腺癌中Stat5a/b的活化预示着疾病早期复发。

The team found that that inhibition of Stat5a/b by antisense oligonucleotides, RNA interference, or adenoviral expression of dominant negative Stat5a/b, kills prostate cancer cells.
研究小组发现通过反义寡核苷酸、RNA干扰或者显著阴性Stat5a/b的腺病毒表达来抑制Stat5a/b可以杀伤前列腺癌细胞。

They also established that inhibition of Stat5a/b attenuates human prostate cancer xenograft tumor growth in nude mice. At 20 days, the Stat5a/b-suppressed mice had tumors 70% smaller than those in controls.
他们也建立了抑制Stat5a/b来缓解裸鼠中人的前列腺癌异种移植肿瘤生长的模型。20天来，Stat5a/b抑制性小鼠的肿瘤体积比对照组缩小了70%。

Therapies for prostate cancer, Dr. Nevalainen said, \"could be achieved by identification of small molecule pharmacological inhibitors for Stat5 -- the molecular mechanism of how Stat5a/b becomes activated provides multiple levels for pharmacological inhibition and therefore drug development.\"
Dr. Nevalainen说：“前列腺癌的治疗可以通过识别Stat5的小分子药物抑制剂来达到。Stat5a/b如何活化的分子机制为药理学抑制和治疗药物的发展提供了多水平的视角。