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Archive > Volume 16 Issue 3 > 2009,16(3):253-257. DOI:10.3872/j.issn.1007-385X.2009.3.009 Prev Next

Basic Research

Hepatocarcinoma specific IL-1β anti sense RNA inhibits implanted hepatocarcinoma in mice

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    Abstract:
    Objective :To construct hepatocarcinoma specific IL1β antisense RNA expression vector and to explore its effect on the growth of implanted hepatocarcinoma H22 cells in mice and the possible mechanism. Methods: Murine IL1β antisense RNA expression vectors pafpIRES2antiIL1β1 and pafpIRES2antiIL1β2 under the regulation of minimal alphafeto protein (AFP) promoter and CMV enhancer were constructed, and further verified by PCR, restriction endonuclease analysis and DNA sequencing. H22 cells transfected with pafpIRES2antiIL1β 1 or pafpIRES2antiIL1β 2 were divided into 3 groups: H22/mock, H22/antiIL1β1 and H22/antiIL1β2 group. Expression of IL1β was detected by RTPCR. Transfected H22 cells were subcutaneously injected into mice to establish tumor implanted mouse model. Tumor volume was measured; the cytotocixity of spleen NK against H22 cells was detected by MTT. Results: Hepatocarcinoma specific IL1β antisense RNA expression vectors pafpIRES2antiIL1β1 and pafpIRES2antiIL1β2 were successfully constructed and were verified by PCR, restriction endonuclease analysis and DNA sequencing. IL1β expression in H22 cells was downregulated after transfected with IL1β antisense RNA expression vectors, especially with the pafpIRES2antiIL1β2 vector. Hepatocarcinoma cells implanted mouse model was successfully established. Tumor volume and growth of tumor in H22/antiIL1β2 mice was obviously smaller than that in H22/mock mice, and the cytotocixity of spleen NK against H22 cells in H22/antiIL1β1 and H22/antiIL1β2 mice was also greatly enhanced. Conclusion: Hepatocarcinoma specific IL1β antisense RNA expression vector pafpIRES2antiIL1β was successfully constructed. It effectively inhibits the growth of implanted hepatocarcinoma in mice probably through specifically blocking expression of IL1β and increasing cytotocixity of spleen NK.

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    Project Supported:
    Supported by the National Natural Science Foundation of China (No.30772497); the “1021” Engineering Foundation of Shandong Public Health System; the Major Science and Technology Project of the Ministry of Education of China (No.205090); the Science and T

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