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Back台大研究發現TXNDC5調控腫瘤纖維化關鍵機制，提升大腸直腸癌免疫治療反應
台大研究發現TXNDC5調控腫瘤纖維化關鍵機制，提升大腸直腸癌免疫治療反應
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自由时报1 hour agoHealth2 min readChinaView translation

台大研究發現TXNDC5調控腫瘤纖維化關鍵機制，提升大腸直腸癌免疫治療反應

台大TXNDC5腫瘤纖維化

Quick Look

國立台灣大學研究團隊發現內質網蛋白TXNDC5促使癌症相關成纖維細胞持續活化，加劇腫瘤纖維化並形成屏障阻擋T細胞進入，剔除TXNDC5可抑制腫瘤生長並提升PD-1免疫治療效果，為改善大腸直腸癌免疫治療抗藥性提供新方向。

AI-generated summary

Why It Matters

大腸直腸癌接受免疫治療時，部分腫瘤因高度纖維化形成屏障，阻礙T細胞進入導致治療抗藥性，是免疫治療效果不佳的重要原因。

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2026/10/03 09:52

台大研究發現TXNDC5調控腫瘤纖維化關鍵機制，提升大腸直腸癌免疫治療反應。圖為內質網蛋白TXNDC5 造成大腸直腸癌惡化之機制。（記者林曉雲翻攝）

〔記者林曉雲／台北報導〕大腸直腸癌接受免疫治療，為何有些腫瘤就是難以攻破？國立台灣大學醫學院藥理學研究所教授楊鎧鍵研究團隊找到關鍵機制，發現內質網蛋白「TXNDC5」會促使癌症相關成纖維細胞持續活化，加劇腫瘤纖維化，如同築起一道屏障，阻擋負責殺死癌細胞的T細胞進入；動物實驗發現，剔除TXNDC5後，不僅可抑制腫瘤生長，也能明顯提升PD-1免疫治療效果，為未來改善大腸直腸癌免疫治療抗藥性提供新方向。

研究成果已於今（2026）年6月5日發表於國際期刊「Nature Communications」。研究團隊指出，「間質型」大腸直腸癌具有高度纖維化的腫瘤微環境，癌症相關成纖維細胞（CAF）會形成緻密纖維化屏障，不僅壓迫腫瘤內血管、造成缺氧，也會阻礙毒殺性T細胞進入腫瘤，是造成免疫治療抗藥性的重要原因之一。

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研究團隊分析人類及小鼠大腸直腸癌資料後發現，TXNDC5在癌症相關成纖維細胞中異常大量表現。進一步追查機制發現，腫瘤微環境中的TGFβ1訊號及內質網壓力會誘導TXNDC5增加，TXNDC5則會維持TGFβ受體TGFBR1的蛋白穩定性，使相關訊號持續作用，進一步促使成纖維細胞活化及腫瘤纖維化，形成惡性循環。

高度纖維化不只是讓腫瘤「變硬」。研究顯示，纖維化會壓迫血管並造成缺氧，進一步形成免疫抑制環境，招募骨髓來源抑制性細胞（MDSCs）、調節型T細胞（Tregs）等免疫耐受細胞，同時把具有殺傷能力的T細胞排除在腫瘤之外，使癌細胞更容易逃避免疫系統攻擊。

研究團隊進一步在小鼠模型中，專一性剔除成纖維細胞的Txndc5，結果腫瘤組織硬度下降，血管受到壓迫及缺氧情形改善，促進腫瘤的發炎型成纖維細胞也隨之減少，毒殺性T細胞則增加進入腫瘤。

更重要的是，改變腫瘤微環境後，不僅能抑制腫瘤生長，也顯著提升阻斷PD-1免疫治療的反應。研究由第一作者程凱琳及合作團隊共同完成，揭示TXNDC5－TGFBR1軸在腫瘤纖維化及免疫治療抗藥性扮演的重要角色，未來可望成為間質型大腸直腸癌調控腫瘤微環境及提升免疫治療效果的新研究方向。

What to Watch

AI outlook — possibilities, not facts

  • TXNDC5將成為間質型大腸直腸癌的新藥物靶標，預計未來幾年將進入前臨床及臨床試驗階段。

    Likely · Within years

Open Questions

  • TXNDC5抑制劑的藥物開發進度如何？
  • 此機制是否適用於其他類型纖維化腫瘤？
  • 人體臨床試驗何時開始？

Related Topics

台大
People楊鎧鍵程凱琳林曉雲
Organizations國立台灣大學醫學院藥理學研究所自由健康網
Places台灣台北
TopicsTXNDC5腫瘤纖維化大腸直腸癌免疫治療PD-1TGFβ1
This article was originally published by 自由时报.

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