WEKO3
アイテム
Major histocompatibility complex class I chain-related gene A and B expression induced by heavy ion beam irradiation in cervical cancer cells
https://repo.qst.go.jp/records/2002009
https://repo.qst.go.jp/records/2002009f2020ff6-217e-47d2-a161-42c6aaffd11f
| アイテムタイプ | 会議発表用資料 / Presentation(1) | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| 公開日 | 2025-05-02 | |||||||||
| タイトル | ||||||||||
| タイトル | Major histocompatibility complex class I chain-related gene A and B expression induced by heavy ion beam irradiation in cervical cancer cells | |||||||||
| 言語 | en | |||||||||
| 言語 | ||||||||||
| 言語 | eng | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6670 | |||||||||
| 資源タイプ | conference poster | |||||||||
| 著者 |
Hasegawa Sumitaka
× Hasegawa Sumitaka
× Nakajima Nakako
|
|||||||||
| 抄録 | ||||||||||
| 内容記述 | Major histocompatibility complex class I chain-related gene A and B (MIC) are transmembrane glycoproteins to function as a ligand for human NKG2D that is a main activating receptor of NK cells. MIC are minimally expressed on normal cells, but frequently upregulated via viral infection, cellular stress signals, and malignant transformation. NKG2D recognizes MIC, resulting in the activation of NK cells. Recent progress on radiation biophysics has shown that radiation can modulate anti-tumor immunity in host irradiated via regulation of immune recognition protein expression on cancer cells. The aim of this study is to investigate the effects of heavy ions beam irradiation on membrane MIC expression in human cervical cancer cells. We used HEK293 cells stably overexpressing HPV-E6 or E7 oncoproteins and 5 human cervical cancer cell lines in this study. Carbon ions beam irradiation (CIR, 290 MeV/n; LET, ∼70 keV/μm, mono peak), a beam of heavy ion beams, was performed at the in-house synchrotron accelerator that is able to produce carbon ion beams. Irradiated doses ranged from 0 to 10 Gy of carbon-ions. Cell membrane MIC expression was evaluated by flowcytometry using an anti-MIC antibody. MIC expression was upregulated in HPV-E6 or E7 overexpressing HEK293 cells and 5 human cervical cancer cells in a dose-dependent manner. HPV16-positive human cervical cancer Caski and cells showed a remarkable upregulation of MIC expression after CIR. Other cervical cell lines (ME-180, HeLa, SiHa, and C33A) showed a modest upregulation. E6- or E7-overexpressing HEK293 cells exhibited a considerable induction of MIC after CIR. We investigated the impact of DNA damage responses on HIR-mediated MIC upregulation using drug inhibitors of proteins that are involved in DNA damage responses. Both pharmacological Chk1 inhibition and ATM inhibition cancelled CIR-mediated MICA/B upregulation in HPV oncoprotein-positive HEK293 cells. The results indicated that ATM/ATR pathways were involved in MIC upregulation on HPV-positive cells including cervical cancer cells. These findings support the favorable combination of MICA/B-targeted therapy with heavy ion therapy against cervical cancers. | |||||||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||||||
| 内容記述 | AACR ANNUAL MEETING 2025 | |||||||||
| 発表年月日 | ||||||||||
| 日付 | 2025-04-28 | |||||||||
