| 黎凯恺,张远威,张念杰,尹 硕,何 念,万 磊,陈 旭,杨雪峰.环境雌激素壬基酚通过 SRXN1 促进结直肠癌细胞增殖、侵袭和迁移的作用研究[J].中国比较医学杂志,2023,33(1):61~69. |
| 环境雌激素壬基酚通过 SRXN1 促进结直肠癌细胞增殖、侵袭和迁移的作用研究 |
| Effects of xenoestrogen nonylphenol on proliferation, invasion and migration of colorectal cancer cells by SRXN1 |
| 投稿时间：2022-06-20 |
| DOI：10. 3969 / j.issn.1671-7856. 2023. 01. 008 |
| 中文关键词: 结直肠癌 壬基酚 细胞增殖 侵袭及迁移 sulfiredoxin-1 |
| 英文关键词:colorectal cancer nonylphenol cell proliferation invasion and metastasis sulfiredoxin-1 |
| 基金项目: |
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| Author Name | Affiliation | | LI Kaikai | Department of Oncology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, China | | ZHANG Yuanwei | Department of Oncology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, China | | ZHANG Nianjie | Department of Oncology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, China | | YIN Shuo | Department of Oncology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, China | | HE Nian | Department of Oncology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, China | | WAN Lei | Department of Oncology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, China | | CHEN Xu | Department of Oncology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, China | | YANG Xuefeng | Department of Oncology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, China |
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| 中文摘要: |
| 目的 研究环境雌激素壬基酚( nonylphenol, NP)对结直肠癌细胞增殖、侵袭、迁移的影响及其与 SRXN1(sulfiredoxin-1)表达的关系。 方法 利用转录组测序及实时荧光定量聚合酶链反应( qRT-PCR)分析 NP 对 COLO205 细胞中 SRXN1 表达的影响。 通过癌症基因组图谱(the cancer genome atlas, TCGA)及免疫组织化学技术 (IHC)分析 SRXN1 在结直肠癌组织中的表达。利用特异性小干扰 RNA 片段( si-SRXN1)抑制 SRXN1 的表达,NP (10-6 mol / L)干预 24 h,通过 CCK-8、克隆形成、Transwell 实验检测 COLO205 细胞增殖、侵袭及迁移能力的影响,蛋 白印迹(Western blot)检测细胞中 ERK1 / 2、PI3K/ Akt、Wnt / β-catenin 通路激活情况。 结果 转录组测序及 qRT- PCR 分析发现,NP 显著上调 COLO205 细胞中 SRXN1 表达(P<0. 05)。 TCGA 及 IHC 检测分析发现,结直肠癌肿瘤 组织中 SRXN1 的表达均显著高于癌旁组(P<0. 01)。 与 Control 组比较,NP(10-6 mol / L)显著促进 COLO205 细胞活力、促进克隆形成、侵袭及迁移(均 P<0. 01),而 si-SRXN1 组显著抑制细胞增殖、侵袭及迁移的能力(P<0. 01);与 si-SRXN1 组比较,NP 联合 si-SRXN1 组细胞活力(P<0. 01)、克隆形成(P<0. 05)、侵袭(P<0. 01)及迁移(P<0. 01) 显著升高。 与 Control 组比较,NP 组中 ERK1 / 2、PI3K/ Akt、Wnt / β-catenin 通路均被激活(均 P<0. 01),si-SRXN1 组均显著抑制(均 P<0. 01);与 si-SRXN1 组比较,NP+si-SRXN1 组中 ERK1 / 2、PI3K/ Akt、Wnt / β-catenin 通路均显著激活(P<0. 01 或 P<0. 05)。 结论 NP 通过促进 SRXN1 的表达,促进结直肠癌细胞的增殖、侵袭和迁移。 |
| 英文摘要: |
| Objective To investigate the effect of xenoestrogen nonylphenol (NP) on the proliferation, invasion, and migration of colorectal cancer cells and its relationship with sulfiredoxin-1 ( SRXN1 ) expression. Methods Transcriptomic sequencing and qRT-PCR were used to analyze the effect of NP, SRXN1 expression in colorectal cancer cells. SRXN1 expression in colorectal cancer was analyzed by TCGA and immunohistochemistry. After SRXN1 knockdown in colorectal cancer cell line COLO205 by a specific small interfering RNA ( si-SRXN1 ), effects on the activity, proliferation, ROS release, invasion, and migration of NP (10-6 mol / L)-treated COLO205 cells was detected by CCK-8, colony formation, transwell, and invasion assays. ERK1 / 2, PI3K/ Akt and Wnt / β-catenin expression was assessed by Western blot. Results Transcriptome sequencing and qRT-PCR analysis showed that NP significantly upregulated SRXN1 expression in COLO205 cells. TCGA and IHC analysis showed that SRXN1 expression in colorectal cancer tissue samples was significantly higher than that in the paracancerous group (P<0. 01). Compared with control group, NP significantly promoted COLO205 cell viability, colony formation, invasion, and migration (P<0. 01). si-SRXN1 significantly inhibited cell proliferation, invasion, and migration (P< 0. 01). Compared with the si-SRXN1 group, cell viability ( P< 0. 01), colony formation (P<0. 05), invasion (P<0. 01), and migration (P<0. 01) were significantly increased in the NP+si- SRXN1 group. Western blotting showed that, compared with the control group, ERK1 / 2, PI3K/ Akt, and Wnt / β-catenin were significantly increased in the NP group ( all P<0. 01) and significantly decreased in the si-SRXN1 group ( all P< 0. 01). Compared with the si-SRXN1 group, ERK1 / 2, PI3K/ Akt and Wnt / β-catenin were significantly increased the in NP+si-SRXN1 group (P<0. 05 or P<0. 01). Conclusions NP promotes the proliferation, invasion, and metastasis of colorectal cancer cells by promoting SRXN1 expression. |
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