肿瘤细胞治疗研究
英文原题：Targeting Reactive Species Stress and Nutrient Sensing to Enhance NK-Cell Function: Mechanistic Strategies for Overcoming Pancreatic Cancer Progression and Resistance Through Supplement Therapy.
Targeting Reactive Species Stress and Nutrient Sensing to Enhance NK-Cell Function: Mechanistic Strategies for Overcoming Pancreatic Cancer Progression and Resistance Through Supplement Therapy.
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胰腺导管腺癌（PDAC）仍然是全球最致命的恶性肿瘤之一，其原因在于诊断延迟、快速转移进展、深度免疫抑制以及治疗反应有限。胰腺肿瘤微环境的特征包括严重缺氧、间质促纤维增生、代谢应激和氧化失衡，这些因素均促进肿瘤进展和治疗耐药。在参与抗肿瘤防御的免疫细胞中，自然杀伤（NK）细胞通过直接细胞毒作用和细胞因子产生发挥重要作用。然而，在PDAC中，由于氧化应激、营养可用性改变、线粒体功能障碍以及AMPK和mTOR等信号通路失调，NK细胞活性经常受损。本综述审视了关于氧化还原生物学、营养感知、NK细胞代谢与胰腺癌进展之间相互作用的当前证据。重要的是，现有证据大多来自体外研究、动物模型或早期临床研究，且若干发现仍存在争议或不一致。需要进一步精心设计的临床试验，以确定营养干预、维生素补充以及靶向代谢和氧化还原通路的策略能否安全有效地增强NK细胞功能并改善PDAC患者的临床结局。
Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest malignancies worldwide because of delayed diagnosis, rapid metastatic progression, profound immune suppression, and limited therapeutic responsiveness.
The pancreatic tumor microenvironment is characterized by severe hypoxia, stromal desmoplasia, metabolic stress, and oxidative imbalance, all of which contribute to tumor progression and resistance to therapy. Among immune cells involved in antitumor defense, natural killer (NK) cells play an important role through direct cytotoxicity and cytokine production.
However, NK-cell activity is frequently impaired in PDAC due to oxidative stress, altered nutrient availability, mitochondrial dysfunction, and dysregulated signaling pathways such as AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR). This review examines current evidence regarding the interactions among redox biology, nutrient sensing, NK-cell metabolism, and pancreatic cancer progression.
Importantly, much of the available evidence derives from in vitro studies, animal models, or early-phase clinical investigations, and several findings remain controversial or inconsistent.
Further well-designed clinical trials are needed to determine whether nutritional interventions, vitamin supplementation, and strategies targeting metabolic and redox pathways can safely and effectively enhance NK-cell function and improve clinical outcomes in patients with PDAC.
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