CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题：CIK-augmented anti-PD1/CTLA4 immunotherapy eradicates chemo-resistant ovarian cancer via tripartite mechanistic synergy.
CIK-augmented anti-PD1/CTLA4 immunotherapy eradicates chemo-resistant ovarian cancer via tripartite mechanistic synergy.
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免疫检查点抑制剂（ICIs）联合过继性细胞治疗是治疗卵巢癌的有前景的策略，但其协同机制仍未得到充分探索。本研究评估了Nivolumab/Ipilimumab联合细胞因子诱导的杀伤（CIK）细胞在卵巢癌模型中的治疗效果。
人卵巢癌细胞（A2780/SKOV3）接受三种处理条件：未处理对照、双免疫检查点抑制剂（ICIs：4 μg/mL Nivolumab + 4 μg/mL Ipilimumab），或ICIs联合CIK细胞（5×10 4 cells/insert），并通过综合实验评估功能影响，包括CCK-8增殖、transwell侵袭、Annexin V-FITC/PI凋亡检测、基于碘化丙啶的细胞周期分析以及定量伤口愈合迁移评估。
三联疗法表现出协同疗效，在matrigel-transwell实验中显著抑制SKOV3细胞增殖达62.3%（P<0.001），并抑制侵袭能力达71.5%（P<0.01）。同时，该疗法在A2780细胞中诱导显著凋亡（增加3.2倍，22.8% vs 对照组7.1%），在SKOV3中引发明显的G0/G1期阻滞（55% vs 对照组40%），并伴随S期减少，在联合治疗组中抑制伤口闭合能力达64.7%。
三联组合疗法通过强效阻断G1/S检查点、对ICI耐药群体选择性细胞毒性以及抑制迁移活性，协同增强抗肿瘤疗效，从而确立CIK-ICI联合给药作为晚期卵巢恶性肿瘤的临床可转化策略。
Immune checkpoint inhibitors (ICIs) combined with adoptive cell therapy represent promising strategies against ovarian cancer, yet their synergistic mechanisms remain underexplored. This study evaluated the therapeutic efficacy of Nivolumab/Ipilimumab plus Cytokine-Induced Killer (CIK) cells in ovarian carcinoma models.
Human ovarian cancer cells (A2780/SKOV3) were subjected to three treatment conditions: untreated controls, dual immune checkpoint inhibitors (ICIs: 4 μg/mL Nivolumab + 4 μg/mL Ipilimumab), or ICIs combined with CIK cells (5×10 4 cells/insert), with functional impacts evaluated through comprehensive assays including CCK-8 proliferation, transwell invasion, Annexin V-FITC/PI apoptosis detection, propidium iodide-based cell cycle analysis, and quantitative wound healing migration assessment.
The triple-combination therapy demonstrated synergistic efficacy, significantly reducing SKOV3 cell proliferation by 62.3% (P<0.001) and suppressing invasion capacity by 71.5% (P<0.01) in matrigel-transwell assays. Concurrently, it induced substantial apoptosis in A2780 cells (3.2-fold increase, 22.8% vs 7.1% control), triggered pronounced G0/G1 phase arrest in SKOV3 (55% vs 40% control) with concomitant S-phase depletion, and inhibited wound closure capacity by 64.7% in combinatorial treatment groups.
The triple-combination therapy synergistically enhances antitumor efficacy through potent G1/S checkpoint blockade, selective cytotoxicity against ICI-resistant populations, and migration-inhibitory activity, thus establishing CIK-ICI coadministration as a clinically translatable strategy for advanced ovarian malignancies.
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