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Local irradiation with 8?Gy was administered every other day for a total of three times, followed by detection of melanoma tumour growth as shown in Figure?4a. Tumours grew rapidly in the pEgr1 and pEgr1-HtrA2 groups. In the pEgr1 with RT group and alone RT group, transient regressions of tumours were observed, but tumours finally regrew in the first 20 days after treatment. In the pEgr1-HtrA2 combined with RT group, the size of the tumours consistently decreased after day 10, and tumour regrowth was not observed on day 40. Moreover, tumour was not observed on day 40 in some mice. A significant difference (P?[http://www.selleckchem.com/products/pexidartinib-plx3397.html Pexidartinib in vivo] in tumour size was observed between treatment with pEgr1-HtrA2 combined with RT group and other groups. To study the radiosensitivity of pEgr1-HtrA2 combined with RT, we analysed another two tumour-bearing nude mice groups (n?=?8) treated with pEgr1-HtrA2 combined with a lower dose of RT (4?Gy/day or a total 12?Gy dose of RT). Tumour growth was also observed (Fig.?4b). In the pEgr1-HtrA2 combined with 4?Gy dose RT group, there is no remarkable increase and regrowth in tumour size. Tumour was not observed on day 30 in one mouse. Considering these results, we believe that the treatment combined with HtrA2 gene and RT could enhance the radiosensitivity of OCM-1 cells in vivo. This proposed therapy can provide a more stable antitumour growth effect on UM tumour than RT alone in vivo. RT is a widely used local and regional modality for the treatment of cancer. However, one of the main [http://www.selleckchem.com/products/SRT1720.html SRT1720 mw] disadvantages is their complete reliance on dose escalation, which makes it impossible to achieve sufficient dose to eradicate radioresistant tumours without unacceptable acute and late normal tissue toxicity.[14] Cancer gene therapy has been a promising but difficult approach.[15, 16] However, one important limitation of gene therapy is still the lack of tumour specificity. In addition, there are always side-effects due to the lack of specificity of antitumour effect in tumour therapies. It is important to find therapeutic approaches that not only specifically enhance [http://en.wikipedia.org/wiki/FKBP FKBP] the radiosensitivity of tumour cells, but also restrict therapeutic gene expression to the tumour cells. In this report, we have demonstrated that transfection of the proapoptotic gene HtrA2, via Egr1-mediated gene delivery system, will sensitize UM cells and tumours to the cytotoxic effects of radiation. To this end, an Egr1-mediated recombinant plasmid containing the HtrA2 gene was constructed.[13] Liposome is often used to transfect plasmids into tumour cells because it has been proven a safe and effective approach in tumour therapy.[17, 18] Furthermore, it is not necessary to have all the tumour cells transfected with the desired gene. Only a few transfected cells would be enough to enable the product of expression to make a difference.