Cancer Research:放疗激活新途径 让前列腺癌治疗更有效
生物谷 · 2015/12/24
最近一项研究发现两种常用的前列腺癌治疗方法在分子层面存在重要联系,这一发现或可帮助病人更加轻松地杀死前列腺癌细胞。


最近一项研究发现两种常用的前列腺癌治疗方法在分子层面存在重要联系,这一发现或可帮助病人更加轻松地杀死前列腺癌细胞。科学家正在研发可以利用这种关联进行癌细胞杀伤的药物,未来将进行临床研究检测这一发现是否能够帮助治疗前列腺癌。

文章作者还表示,这项发现还可能帮助医生更好地确定哪种治疗方法对病人最有利,同时可能对其他类型癌症的治疗也有一定提示。

目前,治疗前列腺癌的常用方法主要包括放射和雄激素消融,而来自弗吉尼亚大学医学院的研究人员发现这两种方法之间存在一种新联系,这是之前所有研究都没有发现的。研究人员发现放射治疗不仅能够抑制细胞分裂,对癌细胞DNA进行损伤,还能够激活一条细胞信号途径,调节细胞对雄激素的敏感性,并会反过来影响前列腺癌细胞对放射治疗的易感性。

文章作者表示:"我们在这两种治疗晚期前列腺癌病人的常用方法之间找到了新的联系。对于未发生转移的晚期前列腺癌,放射治疗是标准疗法之一,放疗不仅会诱导DNA损伤,还会激活这条信号通路,另外一种治疗转移性前列腺癌的标准疗法是雄激素消融,这种方法能够抑制雄激素受体的活性。通过这项研究我们在分子层面上对于这两种不同的治疗方法如何联系在一起有了更进一步的认识。"

了解这些信息,医生就能够通过药物改变这条信号途径--检查点激酶2(CHK2),让前列腺癌的治疗更简单。阻断这条信号,就可以让癌细胞对放射治疗更加易感。

目前一些大的制药公司已经开发用于抑制CHK激酶活性的药物,文章作者希望这项新发现能够推动进一步的临床检测,为前列腺癌人提供更好的治疗方法。

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    Prostate cancer is the second leading cause of cancer death in American men, and curing metastatic disease remains a significant challenge. Nearly all patients with disseminated prostate cancer initially respond to androgen deprivation therapy (ADT), but virtually all patients will relapse and develop incurable castration-resistant prostate cancer (CRPC). A high-throughput RNAi screen to identify signaling pathways regulating prostate cancer cell growth led to our discovery that checkpoint kinase 2 (CHK2) knockdown dramatically increased prostate cancer growth and hypersensitized cells to low androgen levels. Mechanistic investigations revealed that the effects of CHK2 were dependent on the downstream signaling proteins CDC25C and CDK1. Moreover, CHK2 depletion increased androgen receptor (AR) transcriptional activity on androgen-regulated genes, substantiating the finding that CHK2 affects prostate cancer proliferation, partly, through the AR. Remarkably, we further show that CHK2 is a novel AR-repressed gene, suggestive of a negative feedback loop between CHK2 and AR. In addition, we provide evidence that CHK2 physically associates with the AR and that cell-cycle inhibition increased this association. Finally, IHC analysis of CHK2 in prostate cancer patient samples demonstrated a decrease in CHK2 expression in high-grade tumors. In conclusion, we propose that CHK2 is a negative regulator of androgen sensitivity and prostate cancer growth, and that CHK2 signaling is lost during prostate cancer progression to castration resistance. Thus, perturbing CHK2 signaling may offer a new therapeutic approach for sensitizing CRPC to ADT and radiation.

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