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RISS 인기검색어
- 검색키워드
- 저자 : Guruprasath, Padmanaban (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
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Guruprasath, Padmanaban,Kim, Jihoon,Gunassekaran, Gowri Rangaswamy,Chi, Lianhua,Kim, Soyoun,Park, Rang-Woon,Kim, Sang-Hyun,Baek, Moon-Chang,Bae, Sang Mun,Kim, Sang-Yeob,Kim, Dong-Kyu,Park, In-Kyu,Kim, Elsevier 2017 Biomaterials Vol.142 No.-
<P><B>Abstract</B></P> <P>IL-4 receptor (IL-4R) is commonly up-regulated on tumor cells, and interactions between the receptor and Interleukin-4 (IL-4) can induce the expression of anti-apoptotic proteins, including Bcl-xL. This contributes to tumor cell survival and their resistance to chemotherapy. In this study, we exploited IL-4R-targeted delivery of Bcl-xL siRNA to IL-4R-expressing tumor cells in order to sensitize them to chemotherapy. To target IL-4R, an IL-4R-binding peptide, IL4RPep-1, was attached to branched polyethyleneimine-superparamagnetic iron oxide nanoparticles (BPEI-SPION). These nanoparticles were then complexed with Bcl-xL-targeting siRNA. IL-4R-targeted BPEI-SPION/Bcl-xL siRNA more efficiently reduced Bcl-xL gene expression and enhanced cytotoxicity of doxorubicin in MDA-MB231 breast tumor cells compared to untargeted BPEI-SPION/Bcl-xL siRNA. The siRNA was released from the complexes after 15 h of incubation at pH 5.5 and was stable in the complexes up to 72 h in the serum. The IL-4R-targeted BPEI-SPION/siRNA was internalized by cells through IL-4R, successfully escaped the endosomes, and was dispersed into the cytoplasm. Near-infrared fluorescence and magnetic resonance imaging demonstrated that <I>in vivo</I> tumor homing and accumulation of IL-4R-targeted BPEI-SPION/siRNA were both higher than untargeted BPEI-SPION/siRNA. The IL-4R-targeted BPEI-SPION/Bcl-xL siRNA, in combination with doxorubicin, significantly inhibited tumor growth in mice compared to untargeted BPEI-SPION/Bcl-xL siRNA. These results suggest that the IL-4R-targeted delivery of Bcl-xL siRNA to IL-4R-expressing tumors can sensitize tumors to chemotherapy and enhance the efficacy of anti-tumor therapeutics.</P> <P><B>Graphical abstract</B></P> <P>Interaction between IL-4 and IL-4R provides downstream signaling for the expression of Bcl-xL and inhibits doxorubicin-induced apoptosis. IL4RPep-1-labeled BPEI-SPION/Bcl-xL siRNA selectively binds to IL-4R-expressing tumor cells and is internalized into the cells through the receptor-mediated endocytosis, which contributes to the silencing of the Bcl-xL gene expression. This sensitizes IL-4R-expressing tumor cells to doxorubicin and enhances its therapeutic efficacy.</P> <P>[DISPLAY OMISSION]</P>
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Gunassekaran, Gowri Rangaswamy,Hong, Chae-Moon,Vadevoo, Sri Murugan Poongkavithai,Chi, Lianhua,Guruprasath, Padmanaban,Ahn, Byung-Cheol,Kim, Ha-Jeong,Kang, Tae Heung,Lee, Byungheon IPC Science and Technology Press 2018 Biomaterials Vol.159 No.-
<P><B>Abstract</B></P> <P>Adoptive transfer of cytotoxic T lymphocytes (CTLs) has been used as an immunotherapy in melanoma. However, the tumor homing and therapeutic efficacy of transferred CTLs against melanoma remain unsatisfactory. Interleukin-4 receptor (IL-4R) is commonly up-regulated in tumors including melanoma. Here, we studied whether IL-4R-targeted CTLs exhibit enhanced tumor homing and therapeutic efficacy against melanoma. CTLs isolated from mice bearing melanomas were non-genetically engineered with IL4RPep-1, an IL-4R-binding peptide, using a membrane anchor composed of dioleylphosphatidylethanolamine. Compared to control CTLs, IL-4R-targeted CTLs showed higher binding to melanoma cells and <I>in vivo</I> tumor homing. They also exerted a more rapid and robust effector response, including increased cytokine secretion and cytotoxicity against melanoma cells and enhanced reprogramming of M2-type macrophages to M1-type macrophages. Moreover, IL-4R-targeted CTLs efficiently inhibited melanoma growth and reversed the immunosuppressive tumor microenvironment. These results suggest that non-genetically engineered CTLs targeting IL-4R have potential as an adoptive T cell therapy against melanoma.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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