靶向K562肿瘤细胞的1,3,4-噁二唑衍生物的合成、抗癌活性评价及初步作用机制研究

doi:10.6023/cjoc202601044

有机化学 ›› 2026, Vol. 46 ›› Issue (10): 4034-4049.DOI: 10.6023/cjoc202601044 上一篇下一篇

研究论文

靶向K562肿瘤细胞的1,3,4-噁二唑衍生物的合成、抗癌活性评价及初步作用机制研究

吴越友^a, 何丹丹^a, 冯念林^a, 张依^a, 刘丹丹^a, 周玥^a, 李晨晨^a^,^*(), 王贞超^a^,^b^,^*()

^a 贵州大学药学院贵阳 550025
^b 贵州大学精细化工研究开发中心绿色农药全国重点实验室绿色农药与农业生物工程教育部重点实验室贵阳 550025

收稿日期:2026-03-24 修回日期:2026-05-26 发布日期:2026-06-26
基金资助:
国家自然科学基金(32360689); 贵州省优秀青年学者项目(GCC[2023]072); 国家重点研发计划(2023YFD1400400); 贵州省基础研究计划(自然科学)青年引导(QN[2025]010); 贵州省基础研究计划(自然科学)青年引导(QN[2025]009)

Synthesis, Anticancer Evaluation, and Preliminary Mechanism Study of 1,3,4-Oxadiazole Derivatives Targeting K562 Tumor Cells

Yueyou Wu^a, Dandan He^a, Nianlin Feng^a, Yi Zhang^a, Dandan Liu^a, Yue Zhou^a, Chenchen Li^a^,^*(), Zhenchao Wang^a^,^b^,^*()

^a School of Pharmaceutical Sciences, Guizhou University, Guiyang 550025
^b Key Laboratory of Green Pesticide and Agricultural Bioengineering, Ministry of Education, State Key Laboratory of Green Pesticides, Center for R&D of Fine Chemicals, Guizhou University, Guiyang 550025

Received:2026-03-24 Revised:2026-05-26 Published:2026-06-26
Contact:
^* E-mail: licc@gzu.edu.cn;
zcwang@gzu.edu.cn;
Supported by:
National Natural Science Foundation of China(32360689); Guizhou Provincial Foundation for Excellent Scholars Program(GCC[2023]072); National Key Research and Development Program of China(2023YFD1400400); Youth Guidance Project of the Guizhou Provincial Basic Research Program (Natural Science)(QN[2025]010); Youth Guidance Project of the Guizhou Provincial Basic Research Program (Natural Science)(QN[2025]009)

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摘要/Abstract

慢性粒细胞白血病(CML)是一种以髓系细胞异常增殖为特征的血液系统恶性肿瘤. 由于常规酪氨酸激酶抑制剂耐药性的出现, 开发新型抗肿瘤药物势在必行. 基于具有抗肿瘤潜力的吲哚、1,3,4-噁二唑和苯磺酰胺药效团, 设计合成了30个新型杂化衍生物, 旨在提升活性和选择性. 其中N-(5-(1H-吲哚-3-基)-1,3,4-噁二唑-2-基)-3,4,5-三氟苯磺酰胺(XL-10)对CML K562细胞展现出强效抗增殖作用[IC₅₀=(6.69±0.35) μmol/L]. 机制研究表明, XL-10通过打破氧化还原稳态诱导K562细胞凋亡, 其主要表现为活性氧(ROS)水平升高和线粒体膜电位降低; 流式细胞分析显示, 该化合物通过调控细胞周期蛋白(Cyclin B1)及细胞周期蛋白依赖性激酶(CDK1)等关键周期蛋白, 将细胞阻滞于G2/M期; 蛋白质组学和Western blot实验证实了其对丝裂原活化蛋白激酶(MAPK)和磷脂酰肌醇3-激酶(PI3K)-蛋白激酶B (AKT)信号通路的调节作用. 该研究系统阐明了XL-10的抗肿瘤作用机制, 突显其作为靶向CML治疗先导化合物的开发潜力.

关键词: K562细胞, 抗癌活性, 含氮杂环, 慢性髓性白血病, 1,3,4-噁二唑

Chronic myeloid leukemia (CML) is a hematological malignancy characterized by aberrant myeloid cell proliferation, and the emergence of drug resistance to conventional tyrosine kinase inhibitors necessitates novel antitumor agents. Based on the pharmacophore of indole, 1,3,4-oxadiazole, and benzenesulfonamide, which possess antitumor potential, 30 novel hybrid derivatives were designed and synthesized, aiming to enhance activity and selectivity. Among these compounds, N-(5-(1H-indol-3-yl)-1,3,4-oxadiazol-2-yl)-3,4,5-trifluorobenzenesulfonamide (XL-10) demonstrated potent antiproliferative effects against CML K562 cells, exhibiting an IC₅₀ value of (6.69±0.35) μmol/L. Mechanistic investigations revealed that XL-10 induced apoptosis in K562 cells by disrupting redox homeostasis, as evidenced by elevated reactive oxygen species (ROS) levels and reduced mitochondrial membrane potential. Flow cytometry analysis indicated that XL-10 arrests K562 cells at the G2/M phase through regulation of key cell cycle proteins including Cyclin B1 and Cyclin-dependent kinase 1 (CDK1), while Western blot assays confirmed its modulation of the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase/protein kinase B (PI3K-AKT) signaling pathways. These findings elucidate the antitumor mechanisms of XL-10 and highlight its potential as a promising lead compound for the development of targeted CML therapies.

Key words: K562 cell, anticancer activity, nitrogen-containing heterocycle, chronic myeloid leukemia, 1,3,4-oxadiazole

引用此文

吴越友, 何丹丹, 冯念林, 张依, 刘丹丹, 周玥, 李晨晨, 王贞超. 靶向K562肿瘤细胞的1,3,4-噁二唑衍生物的合成、抗癌活性评价及初步作用机制研究[J]. 有机化学, 2026, 46(10): 4034-4049.

Yueyou Wu, Dandan He, Nianlin Feng, Yi Zhang, Dandan Liu, Yue Zhou, Chenchen Li, Zhenchao Wang. Synthesis, Anticancer Evaluation, and Preliminary Mechanism Study of 1,3,4-Oxadiazole Derivatives Targeting K562 Tumor Cells[J]. Chinese Journal of Organic Chemistry, 2026, 46(10): 4034-4049.

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图/表 11

Figure 1. Design strategy of the target compounds

Scheme 1. Synthetic route of compounds XL-1~XL-20 and WG-1~WG-10

Compd.	Inhibition rate^a/% of 10 μmol/L
Compd.	PC-3	A549	K562	HEK
XL-1	—	14.03±2.81	3.52±2.35	18.47±3.32
XL-2	—	20.97±3.68	6.32±1.36	8.62±1.93
XL-3	34.80±2.15	33.18±3.66	6.51±2.39	4.17±3.58
XL-4	9.49±2.9	18.34±4.23	10.30±1.38	12.19±2.55
XL-5	7.98±4.56	19.32±1.99	26.85±2.01	8.31±2.35
XL-6	6.72±4.65	15.36±0.86	31.41±1.63	-5.18±2.80
XL-7	4.21±2.49	12.82±2.46	15.65±2.51	0.69±0.33
XL-8	12.14±1.25	22.65±10.61	10.63±2.54	7.32±5.36
XL-9	30.86±1.43	24.07±2.96	13.28±2.12	19.30±2.12
XL-10	53.72±1.48	18.63±3.04	87.20±1.79	13.13±2.04
XL-11	—	6.33±3.21	14.57±1.72	20.03±3.32
XL-12	—	16.12±5.06	6.75±0.99	15.69±1.93
XL-13	—	17.41±2.36	10.61±0.32	-23.56±3.58
XL-14	—	15.41±0.92	30.55±1.67	12.27±2.55
XL-15	—	15.32±1.14	38.33±1.06	14.61±2.35
XL-16	—	32.55±1.83	13.60±2.67	-14.77±2.80
XL-17	—	31.87±3.16	8.05±1.58	5.42±0.33
XL-18	35.26±3.19	31.03±3.50	20.24±0.43	6.56±5.36
XL-19	—	15.49±0.29	6.08±1.82	13.04±2.12
XL-20	—	—	5.00±1.26	9.56±2.04
WG-1	12.68±3.36	11.81±1.39	—	23.29±2.98
WG-2	—	13.78±1.68	—	23.80±5.13
WG-3	—	7.72±1.55	—	18.99±4.76
WG-4	—	18.52±3.39	12.94±8.88	22.84±1.46
WG-5	14.71±3.60	20.01±0.38	15.60±7.04	16.43±5.60
WG-6	—	17.62±0.83	10.18±5.98	21.50±0.32
WG-7	10.78±3.59	19.04±1.91	11.23±4.79	22.14±1.75
WG-8	10.03±2.30	13.96±0.97	1.56±3.06	17.83±4.43
WG-9	13.12±5.10	12.08±1.14	25.58±2.34	22.65±3.06
WG-10	29.96±6.66	15.28±1.13	3.24±5.68	17.84±2.60
5-Fu^b	62.46±2.79	54.52±1.31
Ima^c			97.58±0.51

Table 1. Preliminary evaluation of the antitumor activity of the target compounds

Compd.	IC₅₀±SD^a/(μmol•L^-1)
XL-10	6.69±0.35
Ima^b	0.39±0.11

Table 2. IC50 of compound XL-10 for antitumor activity

Figure 2. Analysis of the structure-activity relationship of the target compound

Figure 3. (a~e) Apoptosis detection in K562 cells following 24 h exposure to compound XL-10 using Annexin V-FITC/PI dual-staining flow cytometry (DMSO served as the negative control, while Ima was used as the positive reference), and (f) statistical analysis conducted using one-way ANOVA followed by Dunnett’s multiple comparisons test in GraphPad Prism (****p<0.0001 indicating significant differences)

Figure 4. (a~e) Mitochondrial-membrane-potential detection in K562 cells after 24-h treatment with compound XL-10 by JC-1-staining flow cytometry (DMSO served as the negative control, while Ima was used as the reference compound), and (f) statistical significance determined by one-way ANOVA with Dunnett’s multiple comparisons test using GraphPad Prism (****p<0.0001 indicates highly significant differences)

Figure 5. (a) Intracellular ROS detection in K562 cells after 12-h treatment with compound XL-10 using ROS-specific fluorescent-staining flow cytometry (DMSO served as the negative control, while Ima was used as the positive control), and (b) statistical analysis performed using one-way ANOVA with Dunnett’s multiple comparisons test in GraphPad Prism (**p<0.01, ***p<0.001, and ****p<0.0001 indicating significant increases in ROS generation)

Figure 6. (a~e) Analysis of cell cycle distribution in K562 cells upon 24-hour treatment with compound XL-10 at concentrations of 3, 6, and 12 μmol/L, using cell cycle staining followed by flow cytometry (DMSO served as the negative control, while Ima was used as the reference compound), and (f) statistical analysis conducted using two-way ANOVA with Dunnett’s multiple comparisons test in GraphPad Prism

Figure 7. (a) Number of differentially expressed genes (DEGs) in K562 cells after 24 h XL-10 treatment versus DMSO control, (b) Gene Ontology (GO) enrichment analysis of DEGs (The top 10 significantly enriched GO terms within each domain are highlighted), (c) volcano plot of genome-wide transcriptional variations between XL-10 and DMSO treatment groups, and (d) KEGG pathway enrichment analysis based on quantitative transcriptomic profiling of XL-10-treated K562 cells

Figure 8. Protein expression profiling of K562 cells treated with compound XL-10 (a) Expression changes of apoptosis-associated proteins; (b) expression variations of cell cycle-regulating proteins; (c) alterations of proteins involved in MAPK and PI3K-AKT signaling pathways. All data are expressed as mean±SD from three independent experiments (*p<0.05, ** p<0.001, ***p<0.0001)

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靶向K562肿瘤细胞的1,3,4-噁二唑衍生物的合成、抗癌活性评价及初步作用机制研究

Synthesis, Anticancer Evaluation, and Preliminary Mechanism Study of 1,3,4-Oxadiazole Derivatives Targeting K562 Tumor Cells

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