胰腺癌是消化道常見的惡性腫瘤，以吉西他濱為主的藥物治療目前依舊是胰腺癌患者的必要選擇，但耐藥性大大限制了其效用。吉西他濱與其他藥物聯(lián)合使用可以抑制核糖核苷酸還原酶的表達和活性、上調(diào)脫氧胞苷激酶的表達或增大脫氧胞苷激酶與胞苷脫氨酶的比值，影響細胞周期，促進DNA損傷或抑制其修復(fù)，抑制核因子-κB、磷脂酰肌醇-3-激酶/蛋白激酶B、信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子、核因子E2相關(guān)因子2信號通路，激活細胞自噬途徑，影響上皮-間充質(zhì)轉(zhuǎn)化以增加胰腺癌細胞對吉西他濱的敏感性。綜述了吉西他濱聯(lián)合使用其他藥物增加敏感性的機制，以期為其臨床應(yīng)用提供參考。

Pancreatic cancer is a common malignant tumor in the digestive tract. Gemcitabine based drug therapy is still a necessary choice for patients with pancreatic cancer, but drug resistance greatly limits its effectiveness. Gemcitabine combined with other drugs can inhibit the expression and activity of ribonucleotide reductase, up-regulate the expression of deoxycytidine kinase or increase the ratio of deoxycytidine kinase to cytidine deaminase, affect cell cycle, promote DNA damage or inhibit its repair, inhibit NF-κB, PI3K/Akt, STAT, and Nrf2 signal pathway, activate the cell autophagy pathway, and affect epithelial mesenchymal transformation (EMT) to increase the sensitivity of pancreatic cancer cells to gemcitabine. This article reviews the mechanism of gemcitabine combined with other drugs to increase sensitivity, in order to provide reference for its clinical application.

R969.2

廣西高校中青年教師科研基礎(chǔ)能力提升項目(2023KY0530);廣西科技計劃項目青年創(chuàng)新人才科研專項(桂科AD20238051)