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000303228 1001_ $$0P:(DE-HGF)0$$aLiang, Yingying$$b0$$eFirst author
000303228 245__ $$aRadiotherapy Upregulates the Expression of Membrane-Bound Negative Complement Regulator Proteins on Tumor Cells and Limits Complement-Mediated Tumor Cell Lysis.
000303228 260__ $$aBasel$$bMDPI$$c2025
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000303228 520__ $$aBackground/Objectives: Radiotherapy (RT) is a mainstay of clinical cancer therapy that causes broad immune responses. The complement system is a pivotal effector mechanism in the innate immune response, but the impact of RT is less well understood. This study investigates the interaction between RT and the complement system as a possible approach to improve immune responses in cancer treatment. Methods: Human solid cancer (lung, prostate, liver, breast cancer), lymphoma, and leukemia cells were irradiated using X-rays and treated with polyclonal antibodies or anti-CD20 monoclonal antibodies, respectively. Chromium release assay was applied to measure cell lysis after radiation with or without complement-activating antibody treatment. The expression of membrane-bound complement regulatory proteins (mCRPs; CD46, CD55, CD59), which confer resistance against complement activation, CD20 expression, apoptosis, and radiation-induced DNA double-strand breaks (γH2AX), was measured by flow cytometry. The radiosensitivity of tumor cells was assessed by colony-forming assay. Results: We demonstrate that RT profoundly impacts complement function by upregulating the expression of membrane-bound complement regulatory proteins (mCRPs) on tumor cells in a dose- and time-dependent manner. Impaired complement-mediated tumor cell lysis could thus potentially contribute to radiotherapeutic resistance. We also observed RT-induced upregulation of CD20 expression on lymphoma and leukemic cells. Notably, complement activation prior to RT proved more effective in inducing RT-dependent early apoptosis compared to post-irradiation treatment. While complement modulation does not significantly alter RT-induced DNA-damage repair mechanisms or intrinsic radiosensitivity in cancer cells, our results suggest that combining RT with complement-based anti-cancer therapy may enhance complement-dependent cytotoxicity (CDC) and apoptosis in tumor cells. Conclusions: This study sheds light on the complex interplay between RT and the complement system, offering insights into potential novel combinatorial therapeutic strategies and a potential sequential structure for certain tumor types.
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000303228 650_7 $$2Other$$aCD20
000303228 650_7 $$2Other$$aDNA-damage repair
000303228 650_7 $$2Other$$acomplement activation
000303228 650_7 $$2Other$$acomplement-dependent cytotoxicity (CDC)
000303228 650_7 $$2Other$$amembrane-bound complement regulatory proteins (mCRPs)
000303228 650_7 $$2Other$$aradiosensitivity
000303228 650_7 $$2Other$$aradiotherapy
000303228 650_7 $$2Other$$atiming
000303228 7001_ $$0P:(DE-He78)4eba3fd5702e3a245f0b304e53203b2a$$aMai, Lixin$$b1$$udkfz
000303228 7001_ $$0P:(DE-He78)117dc9df1284caf647d139cc91469e77$$aSchneeweiss, Jonathan$$b2$$udkfz
000303228 7001_ $$0P:(DE-He78)c5a1a98649a7874de0def093eb136262$$aLopez Perez, Ramon$$b3$$udkfz
000303228 7001_ $$aKirschfink, Michael$$b4
000303228 7001_ $$0P:(DE-He78)3291aaac20f3d603d96744c1f0890028$$aHuber, Peter$$b5$$eLast author$$udkfz
000303228 773__ $$0PERI:(DE-600)2527080-1$$a10.3390/cancers17142383$$gVol. 17, no. 14, p. 2383 -$$n14$$p2383$$tCancers$$v17$$x2072-6694$$y2025
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