研究者發現，通過抑制兩種關鍵的抗氧化酶—PRDX6（過氧化還原酶6）和GSTP1（谷胱甘肽S轉移酶π1）就能將惡性神經母細胞瘤細胞轉化為成熟的健康神經元，從而顯著抑制腫瘤的進展。

在對抗兒童癌癥的漫長征程中，瑞典科學家們帶來了一線曙光，近日，一篇發表在國際雜志Proceedings of the National Academy of Sciences上題為“Combined targeting of PRDX6 and GSTP1 as a potential differentiation strategy for neuroblastoma treatment”的研究報告中，來自瑞典卡羅琳學院等機構的科學家們通過研究發現了一種全新的治療神經母細胞瘤的策略，有望徹底改變這種致命兒童癌癥的治療格局。

神經母細胞瘤是一種起源于神經系統未成熟細胞的惡性腫瘤，主要影響嬰幼兒和年幼兒童。據統計，神經母細胞瘤占兒童惡性腫瘤的8%至10%，是嬰幼兒中最常見的非腦部實體瘤。其以侵襲性強、預后差而聞名，尤其是當疾病發生轉移時，患者的生存率急劇下降。傳統的治療方案包括手術、化療、放療和免疫治療的組合，但這些療法往往伴隨著嚴重的副作用，如長期的認知功能障礙。據統計，超過一半的神經母細胞瘤患者在治療后會出現復發，且復發后的治療選擇極為有限，因此，開發更精準、更有效的治療方法一直是科學家們的研究重點。

文章中，研究者發現，通過抑制兩種關鍵的抗氧化酶—PRDX6（過氧化還原酶6）和GSTP1（谷胱甘肽S轉移酶π1）就能將惡性神經母細胞瘤細胞轉化為成熟的健康神經元，從而顯著抑制腫瘤的進展，這一創新療法的核心在于誘導癌細胞分化使其從快速增殖的未分化狀態轉變為功能特化的成熟細胞，這種策略不僅能有效減少腫瘤細胞的數量，還能避免傳統化療藥物對健康細胞的無差別攻擊，從而降低治療的毒副作用。

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圖片來源：ijcasereportsandimages.com

這項研究的亮點在于其獨特的靶點選擇，神經母細胞瘤細胞由于代謝活躍，會產生大量的活性氧（ROS），因此其高度依賴抗氧化系統來維持生存。PRDX6和GSTP1在癌細胞的抗氧化防御中起著關鍵作用，其高表達與疾病進展和患者預后不良密切相關。研究人員通過體外實驗和動物模型驗證了抑制這兩種酶的效果，發現其不僅能誘導部分癌細胞死亡，還能促使存活的細胞分化為成熟的神經元，這些分化后的神經元具有正常神經細胞的功能特征，這就表明這種轉化是功能性的而不僅僅是形態上的改變。

此外，這項研究還具有重要的臨床轉化潛力，其中一種酶抑制劑已經獲得了FDA的孤兒藥認定，用于成人疾病的治療，這一認定不僅證明了該藥物的安全性，還為其在兒童神經母細胞瘤中的臨床試驗鋪平了道路，目前，研究人員計劃將這一策略與現有的免疫治療或低劑量化療相結合來進一步提高治療效果，同時減少長期副作用。

盡管這一發現令人振奮，但在臨床應用之前仍面臨一些挑戰，神經母細胞瘤的異質性復雜，需要進一步研究來確定能預測患者對PRDX6和GSTP1抑制劑反應的生物標志物。此外，分化后的神經元在腫瘤微環境中的長期影響也需要仔細評估來確保其不會重新轉變為癌細胞或對周圍神經組織產生不良影響。

總之，這種通過抑制PRDX6和GSTP1誘導神經母細胞瘤細胞分化的創新療法標志著兒童腫瘤學領域的一次重大突破，其不僅有望改善神經母細胞瘤患者的生存率，還能顯著提高患者的生活質量。隨著臨床試驗的推進，科學家們期待這一療法能夠為更多患有這種致命疾病的兒童帶來希望。（生物谷Bioon.com）

參考文獻：

Judit Lia?o-Pons, Elisa Garde-Lapido, Fenja L. Fahrig, et al.Combined targeting of PRDX6 and GSTP1 as a potential differentiation strategy for neuroblastoma treatment, Proceedings of the National Academy of Sciences (2025). DOI:10.1073/pnas.2427211122.