西鈴替尼是腎細胞癌（RCC）治療的一線藥物。然而，接受西鈴替尼治療的患者在6-15個月後最終會產生藥物抗性，對當前RCC治療構成了巨大的障礙。因此，迫切需要澄清西鈴替尼抗性的機制並開發新的克服策略。本文回顧了基於五個主題的西鈴替尼抗性機制在RCC中的總結，包括旁路或替代途徑的激活、不足的藥物積累、腫瘤微環境、代謝重組和表觀遺傳調節。此外，還介紹了克服RCC中西鈴替尼抗性的現有和潛在生物標記物，以及潛在的治療策略。本文受版權保護，版權所有。

Sunitinib is the first-line drug for renal cell carcinoma (RCC) treatment. However, patients who received sunitinib treatment will ultimately develop drug resistance after 6-15 months, creating a huge obstacle to the current treatment of RCC. Therefore, it is urgent to clarify the mechanisms of sunitinib resistance and develop new strategies to overcome it. In this review, the mechanisms of sunitinib resistance in RCC have been summarized based on five topics: activation of bypass or alternative pathway, inadequate drug accumulation, tumor microenvironment, metabolic reprogramming and epigenetic regulation. Furthermore, present and potential biomarkers, as well as potential treatment strategies for overcoming sunitinib resistance in RCC are illustrated.This article is protected by copyright. All rights reserved.