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中华结直肠疾病电子杂志

中华结直肠疾病电子杂志 ›› 2025, Vol. 14 ›› Issue (04) : 319 -332. doi: 10.3877/cma.j.issn.2095-3224.2025.04.004

论著

双氢青蒿素通过JAK2/STAT3信号通路调节结直肠癌细胞的增殖、迁移、凋亡和免疫相关分子研究
黄菊1, 王猛1,2, 韩冬1,†()   
  1. 1150081　哈尔滨医科大学生物化学与分子生物学教研室
    2310005　杭州，浙江省肿瘤医院结直肠外科
  • 收稿日期:2024-09-18 出版日期:2025-08-25
  • 通信作者: 韩冬
  • 基金资助:
    浙江省医药卫生科技计划(No. 2023RC135，No.2024KY795); 浙江省中医药科技计划(No. 2024ZL303); 浙江省自然科学基金华东医药企业创新发展联合基金项目(No. LHDMY24H070002)

Research on dihydroartemisinin regulates the proliferation, migration, apoptosis and immune-related molecules of colorectal cancer cells through JAK2/STAT3 signaling pathway

Ju Huang1, Meng Wang1,2, Dong Han1,†()   

  1. 1Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin 150081, China
    2Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou 310005, China
  • Received:2024-09-18 Published:2025-08-25
  • Corresponding author: Dong Han
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引用本文：

黄菊, 王猛, 韩冬. 双氢青蒿素通过JAK2/STAT3信号通路调节结直肠癌细胞的增殖、迁移、凋亡和免疫相关分子研究[J/OL]. 中华结直肠疾病电子杂志, 2025, 14(04): 319-332.

Ju Huang, Meng Wang, Dong Han. Research on dihydroartemisinin regulates the proliferation, migration, apoptosis and immune-related molecules of colorectal cancer cells through JAK2/STAT3 signaling pathway[J/OL]. Chinese Journal of Colorectal Diseases(Electronic Edition), 2025, 14(04): 319-332.

目的

观察双氢青蒿素（DHA）对结直肠癌细胞增殖、迁移、凋亡和免疫相关分子的影响，并探究其潜在机制。

方法

将人结直肠癌细胞HCT116细胞和RKO细胞作为研究对象，使用6 umol·L-1的DHA处理HCT116细胞，使用12 umol·L-1的DHA处理RKO细胞，采用CCK8实验检测细胞活性；克隆形成实验检测细胞克隆情况；划痕实验和Transwell实验检测细胞迁移情况；Calcein-AM/PI双染法检测细胞死亡的数量变化；Western blot检测凋亡相关蛋白Bcl-2和Cleaved-caspase3的变化、信号通路蛋白JAK2/p-JAK2和STAT3/p-STAT3的变化、免疫分子PD-L1和CD47的变化；实时荧光定量PCR（qRT-PCR）检测免疫因子PD-L1和CD47在mRNA水平中的变化。

结果

与对照组相比，6.25、12.5、25、50、100 umol·L-1的DHA处理结直肠癌细胞48 h后，随着药物浓度增大和处理时间延长，细胞活性显著降低；DHA处理后细胞增殖受到抑制（HCT116：3.021±0.014 vs. 2.449±0.008，t=8.302，P<0.001；RKO：2.666±0.006 vs. 2.122±0.025，t=11.26，P<0.001）；细胞克隆形成计数显著降低（HCT116：252±6.11 vs. 161.7±3.253，t=13.02，P<0.001；RKO：329.4±9.368 vs. 204±9.818，t=9.241，P<0.001）；细胞迁移能力下降（HCT116：26.29%±0.947% vs. 15.2%±1.409%，t=6.533，P<0.01；RKO：30.59%±1.441% vs. 14.77%±0.39%，t=10.6，P<0.001）；细胞死亡增多（HCT116：37.54%±2.128% vs. 58.74%±1.498%，t=8.145，P<0.01；RKO：23.97%±1.203% vs. 34.02%±2.225%，t=3.973，P<0.05）。Western blot结果显示DHA处理后，Bcl-2蛋白含量下降（HCT116：1.001±0.002 vs. 0.551±0.07，t=6.419，P<0.01；RKO：1.001±0.002 vs. 0.827±0.013，t=12.98，P<0.001），Cleaved-caspase3蛋白含量升高（HCT116：1.001±0.002 vs. 1.344±0.119，t=2.904，P<0.05；RKO：1.001±0.002 vs. 1.515±0.086，t=5.995，P<0.01），PD-L1和CD47蛋白含量下降（HCT116：PD-L1：0.999±0.001 vs. 0.829±0.029，t=5.517，P<0.01，CD47：1.001±0.002 vs. 0.763±0.083，t=4.883，P<0.01；RKO：PD-L1：0.995±0.007 vs. 0.885±0.021，t=2.867，P<0.05，CD47：0.991±0.011 vs. 0.562±0.093，t=4.577，P<0.05），p-JAK2和p-STAT3蛋白含量均下降（HCT116：p-JAK2：1.018±0.019 vs. 0.678±0.066，t=4.901，P<0.01，p-STAT3：0.999±0.002 vs. 0.691±0.092，t=3.351，P<0.05；RKO：p-JAK2：1.018±0.019 vs. 0.475±0.064，t=7.092，P<0.001，p-STAT3：0.999±0.002 vs. 0.488±0.091，t=6.926，P<0.001）。qRT-PCR检测结果显示DHA处理后PD-L1和CD47的mRNA表达下降（HCT116：PD-L1：1.002±0.042 vs. 0.888±0.019，t=4.052，P<0.05，CD47：1±0.003 vs. 0.868±0.014，t=9.098，P<0.001；RKO：PD-L1：1±0.002 vs. 0.671±0.024，t=13.64，P<0.001，CD47：1.011±0.02 vs. 0.727±0.02，t=10.07，P<0.001）。加入JAK2激动剂Coumermycin A1后，抵消了DHA对结直肠癌细胞的抑制作用。

结论

DHA能通过抑制JAK2/STAT3信号通路来抑制结直肠癌细胞增殖、迁移，促进细胞凋亡并调控免疫相关分子。

关键词: 结直肠癌, 双氢青蒿素, 凋亡, 免疫, JAK2/STAT3
Objective

This study investigates the effects of Dihydroartemisinin (DHA) on the proliferation, migration, apoptosis, and immune-related molecules of colorectal cancer cells, along with the underlying mechanisms involved.

Methods

Human colorectal cancer cells HCT116 and RKO were treated with 6 umol·L-1 and 12 umol·L-1of DHA, respectively. Cell viability was detected using the CCK-8 assay; colony formation assay was used to detect cell cloning; wound healing assay and Transwell assay were used to evaluate cell migration; the Calcein-AM/PI double staining was used to assess changes in the number of dead cells; Western blot analysis was used to detect changes in apoptosis-related proteins Bcl-2 and Cleaved-caspase3, signal pathway proteins JAK2/p-JAK2 and STAT3/p-STAT3, and immune factors PD-L1 and CD47. Additionally, quantitative Realtime PCR(qRT-PCR) was performed to measure the changes of immune factors PD-L1 and CD47 at the mRNA level.

Results

Compared with the control group, treatment of HCT116 and RKO cells with DHA at concentrations of 6.25、12.5、25、50、100 umol·L-1 for 48 h results in a significant decrease in cell viability with increasing drug concentration and prolonged treatment duration. Cell proliferation was inhibited by DHA treatment (HCT116: 3.021±0.014 vs. 2.449±0.008, t=8.302, P<0.001; RKO: 2.666±0.006 vs. 2.122±0.025, t=11.26, P<0.001). The cell clone formation count was significantly decreased (HCT116: 252±6.11 vs. 161.7±3.253, t=13.02, P<0.001; RKO: 329.4±9.368 vs. 204±9.818, t=9.241, P<0.001), cell migration ability decreased (HCT116: 26.29%±0.947% vs. 15.2%±1.409%, t=6.533, P<0.01; RKO: 30.59%±1.441% vs. 14.77%±0.39%, t=10.6, P<0.001) and cell death (HCT116: 37.54%±2.128% vs. 58.74%±1.498%, t=8.145, P<0.01; RKO: 23.97%±1.203% vs. 34.02%±2.225%, t=3.973, P<0.05) increased. Western blot results demonstrate that DHA treatment leads to a decrease in Bcl-2 protein levels (HCT116: 1.001±0.002 vs. 0.551±0.07, t=6.419, P<0.01; RKO: 1.001±0.002 vs. 0.827±0.013, t=12.98, P<0.001), an increase in Cleaved-caspase3 protein levels (HCT116: 1.001±0.002 vs. 1.344±0.119, t=2.904, P<0.05; RKO: 1.001±0.002 vs. 1.515±0.086, t=5.995, P<0.01), and reductions in PD-L1 and CD47 protein levels (HCT116: PD-L1: 0.999±0.001 vs. 0.829±0.029, t=5.517, P<0.01, CD47: 1.001±0.002 vs. 0.763±0.083, t=4.883, P<0.01; RKO: PD-L1: 0.995±0.007 vs. 0.885±0.021, t=2.867, P<0.05, CD47: 0.991±0.011 vs. 0.562±0.093, t=4.577, P<0.05), along with a reduction in the levels of p-JAK2 and p-STAT3 (HCT116: p-JAK2: 1.018±0.019 vs. 0.678±0.066, t=4.901, P<0.01, p-STAT3: 0.999±0.002 vs. 0.691±0.092, t=3.351, P<0.05; RKO: p-JAK2: 1.018±0.019 vs. 0.475±0.064, t=7.092, P<0.001, p-STAT3: 0.999±0.002 vs. 0.488±0.091, t=6.926, P<0.001). qRT-PCR analysis further shows that DHA treatment results in decreased mRNA expression of PD-L1 and CD47 (HCT116: PD-L1: 1.002±0.042 vs. 0.888±0.019, t=4.052, P<0.05, CD47: 1±0.003 vs. 0.868±0.014, t=9.098, P<0.001; RKO: PD-L1: 1±0.002 vs. 0.671±0.024, t=13.64, P<0.001, CD47: 1.011±0.02 vs. 0.727±0.02, t=10.07, P<0.001). The addition of the JAK2 agonist Coumermycin A1 counteracts the inhibitory effects of DHA on colorectal cancer cells.

Conclusion

DHA can inhibit the proliferation and migration of colorectal cancer cells, promote apoptosis, and regulate immune-related molecules by inhibiting JAK2/STAT3 signaling pathway.

Key words: Colorectal cancer, Dihydroartemisinin, Apoptosis, Immunity, JAK2/STAT3
图1 DHA抑制结直肠癌细胞活力（±s，n=3）。1A：HCT116细胞系的IC50；1B：RKO细胞系的IC50
图2 DHA抑制结直肠癌细胞的增殖（±s，n=3）。2A：CCK8实验显示DHA抑制HCT116细胞的增殖；2B：CCK8实验显示DHA抑制RKO细胞的增殖；2C：克隆形成实验显示DHA抑制HCT116细胞克隆团的形成；2D：HCT116细胞克隆形成数量的统计图；2E：克隆形成实验显示DHA抑制RKO细胞克隆团的形成；2F：RKO细胞克隆形成数量的统计图。***：P<0.001
图3 DHA抑制结直肠癌细胞的迁移（±s，n=3）。3A：划痕实验显示DHA降低HCT116细胞的迁移率；3B：HCT116细胞相对迁移率的统计图；3C：划痕实验显示DHA降低RKO细胞的迁移率；3D：RKO细胞相对迁移率的统计图；3E：Transwell实验显示DHA减少HCT116细胞的迁移个数；3F：HCT116细胞迁移个数的统计图；3G：Transwell实验显示DHA减少RKO细胞的迁移个数；3H：RKO细胞迁移个数的统计图。**：P<0.01，***：P<0.001
图4 DHA促进结直肠癌细胞的凋亡（±s，n=3）。4A：Calcein-AM/PI活细胞/死细胞染色实验显示HCT116细胞死亡数增多；4B：HCT116细胞死亡率的统计图；4C：Calcein-AM/PI活细胞/死细胞染色实验显示RKO细胞死亡数增多；4D：RKO细胞死亡率的统计图；4E：Western blot检测DHA对Bcl-2和Cleaved-caspase3蛋白表达的影响；4F：HCT116细胞Western blot的统计图；4G：RKO细胞Western blot的统计图。*：P<0.05，**：P<0.01，***：P<0.001
图5 DHA抑制免疫检查点分子的表达（±s，n=3）。5A：实时荧光定量PCR检测DHA对PD-L1在mRNA表达的影响；5B：实时荧光定量PCR检测DHA对CD47在mRNA表达的影响；5C：Western blot检测DHA对PD-L1蛋白表达的影响；5D：HCT116细胞Western blot的统计图；5E：RKO细胞Western blot的统计图；5F：Western blot检测DHA对CD47蛋白表达的影响；5G：HCT116细胞Western blot的统计图；5H：RKO细胞Western blot的统计图。*：P<0.05，**：P<0.01，***：P<0.001
图6 DHA抑制JAK2/STAT3通路蛋白的表达（±s，n=3）。6A：Western blot检测DHA对JAK2、p-JAK2、STAT3、p-STAT3蛋白表达的影响；6B：HCT116细胞Western blot的统计图；6C：RKO细胞Western blot的统计图。*：P<0.05，**：P<0.01，***：P<0.001
表1 DHA抑制HCT116细胞后JAK2/STAT3通路蛋白的表达（±s，n=3）
组别 JAK2 p-JAK2 STAT3 p-STAT3
对照组 0.999±0.002 1.018±0.019 1.006±0.009 0.999±0.002
DHA组 0.489±0.111 0.678±0.066 0.652±0.124 0.691±0.092
t值 5.042 3.353 3.492 3.043
P值 <0.001 <0.05 <0.05 <0.05
表2 DHA抑制RKO细胞后JAK2/STAT3通路蛋白的表达（±s，n=3）
组别 JAK2 p-JAK2 STAT3 p-STAT3
对照组 0.999±0.002 1.018±0.019 1.006±0.009 0.999±0.002
DHA组 0.625±0.097 0.475±0.064 0.753±0.007 0.488±0.091
t值 4.709 7.164 2.945 6.752
P值 <0.001 <0.001 <0.05 <0.001
图7 JAK2激动剂Coumermycin A1逆反DHA对结直肠癌细胞的抑制作用（±s，n=3）。7A：克隆形成实验检测加入DHA和Coumermycin A1后细胞克隆团的变化；7B：HCT116细胞克隆形成数量的统计图；7C：RKO细胞克隆形成数量的统计图；7D：Transwell实验检测加入DHA和Coumermycin A1后细胞迁移个数的变化；7E：HCT116细胞迁移个数的统计图；7F：RKO细胞迁移个数的统计图；7G：Western blot检测DHA对JAK2、p-JAK2、STAT3、p-STAT3、PD-L1、CD47和Bcl-2蛋白表达的影响；7H：HCT116细胞Western blot的统计图；7I：RKO细胞Western blot的统计图。*：P<0.05，**：P<0.01，***：P<0.001
表3 JAK2激动剂Coumermycin A1在HCT116细胞中逆反DHA对相关蛋白表达的抑制作用（±s，n=3）
组别 JAK2 p-JAK2 STAT3 p-STAT3 PD-L1 CD47 Bcl-2
对照组 1.000±0.001 0.999±0.001 1.000±0.002 1.003±0.004 0.999±0.014 0.999±0.001 1.000±0.005
DHA组 0.725±0.031 0.414±0.024 0.706±0.107 0.576±0.0341 0.592±0.145 0.459±0.031 0.515±0.042
DHA+Coumermycin A1组 0.598±0.028 0.903±0.051 0.864±0.104 0.971±0.167 1.032±0.095 1.092±0.133 0.848±0.0299
t值 1.780 6.817 2.200 5.510 6.149 8.837 4.654
P值 ns <0.001 ns <0.001 <0.001 <0.001 <0.01
表4 JAK2激动剂Coumermycin A1在RKO细胞中逆反DHA对相关蛋白表达的抑制作用（±s，n=3）
组别 JAK2 p-JAK2 STAT3 p-STAT3 PD-L1 CD47 Bcl-2
对照组 1.000±0.001 0.999±0.001 1.000±0.002 1.003±0.004 0.999±0.014 0.999±0.001 1.000±0.005
DHA组 0.674±0.065 0.382±0.050 0.793±0.103 0.354±0.024 0.455±0.0431 0.332±0.019 0.369±0.035
DHA+Coumermycin A1组 0.636±0.115 0.959±0.063 0.950±0.021 1.040±0.015 1.042±0.095 0.905±0.074 0.822±0.060
t值 0.726 11.04 3.002 13.13 11.23 10.96 8.660
P值 ns <0.001 ns <0.001 <0.001 <0.001 <0.001
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