% IMPORTANT: The following is UTF-8 encoded. This means that in the presence % of non-ASCII characters, it will not work with BibTeX 0.99 or older. % Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or % “biber”. @ARTICLE{Liang:303228, author = {Y. Liang$^*$ and L. Mai$^*$ and J. Schneeweiss$^*$ and R. Lopez Perez$^*$ and M. Kirschfink and P. Huber$^*$}, title = {{R}adiotherapy {U}pregulates the {E}xpression of {M}embrane-{B}ound {N}egative {C}omplement {R}egulator {P}roteins on {T}umor {C}ells and {L}imits {C}omplement-{M}ediated {T}umor {C}ell {L}ysis.}, journal = {Cancers}, volume = {17}, number = {14}, issn = {2072-6694}, address = {Basel}, publisher = {MDPI}, reportid = {DKFZ-2025-01579}, pages = {2383}, year = {2025}, note = {#EA:E055#LA:E055#}, abstract = {Background/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.}, keywords = {CD20 (Other) / DNA-damage repair (Other) / complement activation (Other) / complement-dependent cytotoxicity (CDC) (Other) / membrane-bound complement regulatory proteins (mCRPs) (Other) / radiosensitivity (Other) / radiotherapy (Other) / timing (Other)}, cin = {E055}, ddc = {610}, cid = {I:(DE-He78)E055-20160331}, pnm = {315 - Bildgebung und Radioonkologie (POF4-315)}, pid = {G:(DE-HGF)POF4-315}, typ = {PUB:(DE-HGF)16}, pubmed = {pmid:40723265}, doi = {10.3390/cancers17142383}, url = {https://inrepo02.dkfz.de/record/303228}, }