英国一项最新研究发现，抑制一个与细胞修复有关的基因发挥作用，有助于用放射疗法杀死癌细胞。
英国牛津大学研究人员在新一期《癌症研究》杂志上报告说，通过放射疗法杀死癌细胞是当前治疗癌症的主要手段之一。有关专家指出，提高癌细胞对放射疗法的敏感性，可使疗效大大提高。
牛津大学研究人员为此筛查了那些与细胞修复有关的基因，并最终确定如果抑制一个名为POLQ的基因发挥作用，将可以使包括喉癌和胰腺癌在内的癌细胞对放射疗法更为敏感，治疗效果更好。
研究还发现，这一基因在健康细胞中并不活跃，抑制其发挥作用后，健康细胞对放射疗法的敏感性并没有太大变化，不会因放射疗法而大批死亡。因此，POLQ基因是提高放射疗法效果的一个良好靶点。
研究人员麦肯纳说，实验显示，抑制该基因发挥作用可以使大量癌细胞在放射疗法实施过程中死亡。他们接下来要做的就是把这一发现转化为实际的医疗手段，以造福癌症患者。(生物谷Bioon.com)
生物谷推荐原文出处：
Cancer Research. doi: 10.1158/0008-5472.CAN-09-4040
A Small Interfering RNA Screen of Genes Involved in DNA Repair Identifies Tumor-Specific Radiosensitization by POLQ Knockdown
Geoff S. Higgins1, Remko Prevo1, Yin-Fai Lee1, Thomas Helleday1, Ruth J. Muschel1, Steve Taylor2, Michio Yoshimura1, Ian D. Hickson3, Eric J. Bernhard1 and W. Gillies McKenna1
Authors' Affiliations: 1 Gray Institute for Radiation Oncology and Biology, 2 Computational Biology Research Group, and 3 Genome Integrity Group, Oxford University, Oxford, United Kingdom
The effectiveness of radiotherapy treatment could be significantly improved if tumor cells could be rendered more sensitive to ionizing radiation (IR) without altering the sensitivity of normal tissues. However, many of the key therapeutically exploitable mechanisms that determine intrinsic tumor radiosensitivity are largely unknown. We have conducted a small interfering RNA (siRNA) screen of 200 genes involved in DNA damage repair aimed at identifying genes whose knockdown increased tumor radiosensitivity. Parallel siRNA screens were conducted in irradiated and unirradiated tumor cells (SQ20B) and irradiated normal tissue cells (MRC5). Using H2AX foci at 24 hours after IR, we identified several genes, such as BRCA2, Lig IV, and XRCC5, whose knockdown is known to cause increased cell radiosensitivity, thereby validating the primary screening end point. In addition, we identified POLQ (DNA polymerase ) as a potential tumor-specific target. Subsequent investigations showed that POLQ knockdown resulted in radiosensitization of a panel of tumor cell lines from different primary sites while having little or no effect on normal tissue cell lines. These findings raise the possibility that POLQ inhibition might be used clinically to cause tumor-specific radiosensitization.
