It has been reported that the expression of Krüppel-like factor 17 (KLF17) was associated with the occurrence, development, invasion, metastasis and chemotherapy resistance of various tumors. However, the detailed mechanisms by which KLF17 promotes chemotherapy resistance in gastric cancer (GC) have not been fully investigated. In the present study, we collected the GC tissues and non-tumor tissues (matched adjacent normal tissues with corresponding GC tissues) of 60 GC patients, used qRT-PCR, Western blot and immunohistochemistry assay to analyze the relationship between the expression of KLF17 and the clinical pathological data of the patients. The effect of KLF17 on the sensitivity of GC cell lines to 5-fluorouracil (5-FU), and the potential mechanism were detected by MTS assay, Flow cytometry assay, and Western blot. Compared with non-tumor tissues, the expression level of KLF17 in GC tissue was significantly down-regulated, and the expression level of KLF17 in GES-1 cell line and GC cell lines also had a similar trend. Down-regulated expression of KLF17 is related to tumor size, invasion, regional lymph node metastasis, and TNM staging. Furthermore, through upregulating the expression of KLF17, the sensitivity of BGC-823 and SGC-7901 cell lines to 5-FU was obviously increased. Mechanistically, upregulation the expression of KLF17 can inhibit the expressions of P-glycoprotein (P-gp), multidrug resistance protein 1 (MRP1), and B-Cell lymphoma-2 (BCL-2), which have been reported to be associated with drug resistance and cell proliferation. Collectively, these data implied that KLF17 has the biological effect of inhibiting chemotherapy resistance of GC, and it could be a potential strategy for the GC chemotherapy resistance.

已有报道Krüppel样因子17（KLF17）的表达与多种肿瘤的发生、发展、侵袭、转移和化疗耐药有关。然而，KLF17 促进胃癌（GC）化疗耐药的详细机制尚未得到充分研究。在本研究中，我们收集了 60 名 GC 患者的 GC 组织和非肿瘤组织（匹配的相邻正常组织与相应的 GC 组织），使用 qRT-PCR、Western blot 和免疫组织化学分析来分析 KLF17 和患者的临床病理资料。KLF17对GC细胞系对5-氟尿嘧啶（5-FU）敏感性的影响，并通过MTS检测、流式细胞术检测和Western blot检测其潜在机制。与非肿瘤组织相比，GC组织中KLF17的表达水平显着下调，GES-1细胞系和GC细胞系中KLF17的表达水平也有相似的趋势。KLF17 的下调表达与肿瘤大小、侵袭、区域淋巴结转移和 TNM 分期有关。此外，通过上调KLF17的表达，BGC-823和SGC-7901细胞系对5-FU的敏感性明显增加。从机制上讲，上调 KLF17 的表达可以抑制 P-糖蛋白 (P-gp)、多药耐药蛋白 1 (MRP1) 和 B 细胞淋巴瘤-2 (BCL-2) 的表达，据报道这些蛋白与耐药性和细胞增殖。总的来说，这些数据暗示KLF17具有抑制GC化疗耐药的生物学作用，