英國一項最新研究發(fā)現(xiàn),，抑制一個與細(xì)胞修復(fù)有關(guān)的基因發(fā)揮作用,，有助于用放射療法殺死癌細(xì)胞。
英國牛津大學(xué)研究人員在新一期《癌癥研究》雜志上報告說,，通過放射療法殺死癌細(xì)胞是當(dāng)前治療癌癥的主要手段之一,。有關(guān)專家指出，提高癌細(xì)胞對放射療法的敏感性,，可使療效大大提高,。
牛津大學(xué)研究人員為此篩查了那些與細(xì)胞修復(fù)有關(guān)的基因，并最終確定如果抑制一個名為POLQ的基因發(fā)揮作用,，將可以使包括喉癌和胰腺癌在內(nèi)的癌細(xì)胞對放射療法更為敏感,，治療效果更好。
研究還發(fā)現(xiàn),，這一基因在健康細(xì)胞中并不活躍,，抑制其發(fā)揮作用后，健康細(xì)胞對放射療法的敏感性并沒有太大變化,，不會因放射療法而大批死亡,。因此，POLQ基因是提高放射療法效果的一個良好靶點,。
研究人員麥肯納說,，實驗顯示，抑制該基因發(fā)揮作用可以使大量癌細(xì)胞在放射療法實施過程中死亡,。他們接下來要做的就是把這一發(fā)現(xiàn)轉(zhuǎn)化為實際的醫(yī)療手段,，以造福癌癥患者。(生物谷Bioon.com)
生物谷推薦原文出處：
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.
