hsa_circ_0001900通过加速G1/S细胞周期转换促进肾母细胞瘤细胞增殖、迁移、侵袭并抑制其凋亡

doi:10.3969/j.issn.1674-8115.2026.06.006

上海交通大学学报（医学版） ›› 2026, Vol. 46 ›› Issue (6): 740-750.doi: 10.3969/j.issn.1674-8115.2026.06.006

• 论著 · 基础研究 • 上一篇

hsa_circ_0001900通过加速G1/S细胞周期转换促进肾母细胞瘤细胞增殖、迁移、侵袭并抑制其凋亡

朱润东, 高志强, 向彬, 洪鹏, 胡再宏, 崔孔孔, 龙腾, 张志军, 马伟, 陈鹏飞, 石秦林, 田小毛(), 魏光辉

重庆医科大学附属儿童医院泌尿外科，儿童少年健康与疾病国家临床医学研究中心，儿童发育疾病研究教育部重点实验室，结构性出生缺陷与器官修复重建重庆市重点实验室，重庆 400014

收稿日期:2025-11-28 接受日期:2026-03-16 出版日期:2026-06-28 发布日期:2026-06-29
通讯作者: 田小毛，主治医师，副研究员，博士；电子信箱：xiao-mao@hospital.cqmu.edu.cn。
基金资助:
国家自然科学基金(82403383);重庆市自然科学基金(CSTB2025NSCQ-GPX1154);中国博士后自然科学基金(2024M753886);重庆市博士后研究项目(2024CQBSHTB3021)

hsa_circ_0001900 enhances the proliferation, migration, and invasion of Wilms tumor cells while suppressing apoptosis through acceleration of G1/S cell cycle transition

Zhu Rundong, Gao Zhiqiang, Xiang Bin, Hong Peng, Hu Zaihong, Cui Kongkong, Long Teng, Zhang Zhijun, Ma Wei, Chen Pengfei, Shi Qinlin, Tian Xiaomao(), Wei Guanghui

Department of Urological Surgery, Children's Hospital of Chongqing Medical University; National Clinical Research Center for Children and Adolescents' Health and Diseases; Ministry of Education Key Laboratory of Child Development and Disorders; Chongqing Key Laboratory of Structural Birth Defect and Reconstruction, Chongqing 400014, China

Received:2025-11-28 Accepted:2026-03-16 Online:2026-06-28 Published:2026-06-29
Contact: Tian Xiaomao, E-mail: xiao-mao@hospital.cqmu.edu.cn.
Supported by:
National Natural Science Foundation of China(82403383);Natural Science Foundation of Chongqing(CSTB2025NSCQ-GPX1154);Postdoctoral Natural Science Foundation of China(2024M753886);Postdoctoral Research Projects of Chongqing(2024CQBSHTB3021)

摘要/Abstract

摘要：

目的·探索环状RNA（circular RNA，circRNA）分子hsa_circ_0001900在肾母细胞瘤中的功能及其潜在机制。方法·应用慢病毒构建稳定过表达hsa_circ_0001900的细胞株（WIT-49、WT-CLS1和SK-NEP-1），并使用特异性小干扰RNA（small interfering RNA，siRNA）对该分子进行瞬时沉默。将hsa_circ_0001900过表达细胞株和对照细胞株行转录组测序，基于差异表达基因集富集分析初步探索其潜在生物学功能。通过细胞计数试剂盒8（cell counting kit-8，CCK-8）法、划痕试验、Transwell实验和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（terminal deoxynucleotidyl transferase dUTP nick end labeling，TUNEL）检测法，评估hsa_circ_0001900对肾母细胞瘤细胞增殖、迁移、侵袭和凋亡的影响。进一步采用基因集富集分析（gene set enrichment analysis，GSEA）和基因集变异分析（gene set variation analysis，GSVA）筛选hsa_circ_0001900可能调控的京都基因和基因组百科全书（Kyoto Encyclopedia of Genes and Genomes，KEGG）信号通路。最后，通过流式细胞术检测细胞周期分布与凋亡情况，对相关通路进行实验验证。结果·PCR实验证实，相对于正常人胚肾HEK-293T细胞，hsa_circ_0001900在肾母细胞瘤细胞系（WIT-49、WT-CLS1和SK-NEP-1）中表达显著上调。通过慢病毒和siRNA分别构建了稳定过表达细胞株和瞬时沉默细胞株，用于后续实验分析。转录组差异基因集富集分析显示，差异基因主要富集在细胞增殖、周期调控、迁移和凋亡等条目上。体外实验进一步证实，过表达hsa_circ_0001900可促进肾母细胞瘤细胞的增殖、迁移和侵袭能力，而沉默该分子则明显抑制上述恶性生物学过程并促进细胞凋亡。机制方面，以hsa_circ_0001900为核心的富集分析显示，GSEA和GSVA共同富集到细胞周期通路。流式细胞术检测发现，hsa_circ_0001900稳定过表达的WIT-49、WT-CLS1和SK-NEP-1细胞中，G1期明显缩短，S期明显延长，提示该分子可能通过促进G1/S期转换驱动肾母细胞瘤恶性进展。结论·hsa_circ_0001900在肾母细胞瘤细胞中特异性高表达。该分子通过加速细胞G1/S期转换，促进肾母细胞瘤细胞增殖、迁移、侵袭并抑制细胞凋亡。

关键词: 肾母细胞瘤, 环状RNA, hsa_circ_0001900, 细胞周期

Abstract:

Objective ·To explore the function and potential mechanism of circular RNA (circRNA) hsa_circ_0001900 in Wilms tumor. Methods ·Lentivirus was used to construct cell lines with stable overexpression of hsa_circ_0001900 (WIT-49, WT-CLS1, and SK-NEP-1), and specific small interfering RNA (siRNA) was used to transiently silence this molecule. Transcriptome sequencing was performed on hsa_circ_0001900-overexpressing and control cell lines, and its potential biological functions were preliminarily explored based on enrichment analysis of differentially expressed genes. cell counting kit-8 (CCK-8) assay, wound-healing assay, Transwell assay, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay were used to evaluate the effects of hsa_circ_0001900 on the proliferation, migration, invasion, and apoptosis of Wilms tumor cells. Gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA) were further adopted to screen Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways potentially regulated by hsa_circ_0001900. Finally, flow cytometry was used to detect cell cycle distribution and apoptosis to verify the related pathways experimentally. Results ·PCR assays confirmed that the expression of hsa_circ_0001900 was significantly upregulated in Wilms tumor cell lines (WIT-49, WT-CLS1, and SK-NEP-1) compared with normal human embryonic kidney HEK-293T cells. Cell lines with stable overexpression and transient silencing were successfully constructed using lentivirus and siRNA, respectively. Enrichment analysis of transcriptomic data showed that differentially expressed genes were mainly enriched in pathways associated with cell proliferation, cell cycle regulation, migration, and apoptosis. In vitro experiments further confirmed that overexpression of hsa_circ_0001900 promoted the proliferation, migration, and invasion of Wilms tumor cells, while silencing this molecule significantly inhibited the above malignant biological behaviors and induced cell apoptosis. Mechanistically, enrichment analysis centered on hsa_circ_0001900 revealed that GSEA and GSVA jointly enriched the cell cycle signaling pathway. Flow cytometry detection showed that stable overexpression of hsa_circ_0001900 markedly shortened the G1 phase and prolonged the S phase in WIT-49, WT-CLS1, and SK-NEP-1 cells, suggesting that this molecule may drive the malignant progression of Wilms tumor by facilitating G1/S phase transition. Conclusion ·hsa_circ_0001900 is specifically highly expressed in Wilms tumor cells. This molecule promotes the proliferation, migration, and invasion of Wilms tumor cells and inhibits cell apoptosis by accelerating the G1/S cell cycle transition.

Key words: Wilms tumor, circular RNA (circRNA), hsa_circ_0001900, cell cycle

中图分类号:

R726.9

朱润东, 高志强, 向彬, 洪鹏, 胡再宏, 崔孔孔, 龙腾, 张志军, 马伟, 陈鹏飞, 石秦林, 田小毛, 魏光辉. hsa_circ_0001900通过加速G1/S细胞周期转换促进肾母细胞瘤细胞增殖、迁移、侵袭并抑制其凋亡[J]. 上海交通大学学报（医学版）, 2026, 46(6): 740-750.

Zhu Rundong, Gao Zhiqiang, Xiang Bin, Hong Peng, Hu Zaihong, Cui Kongkong, Long Teng, Zhang Zhijun, Ma Wei, Chen Pengfei, Shi Qinlin, Tian Xiaomao, Wei Guanghui. hsa_circ_0001900 enhances the proliferation, migration, and invasion of Wilms tumor cells while suppressing apoptosis through acceleration of G1/S cell cycle transition[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026, 46(6): 740-750.

图/表 8

表1 特异性沉默hsa_circ_0001900的siRNA序列

Tab 1 siRNA sequences used for specific silencing of hsa_circ_0001900

siRNA	Target sequence(5'→3')
siRNA-1 (si-hsa_circ_0001900-1)	CTGGATCAACAAGATAACA
siRNA-2 (si-hsa_circ_0001900-2)	TCAACAAGATAACATCCCT
siRNA-3 (si-hsa_circ_0001900-3)	CAAGATAACATCCCTGAGG

图1 使用慢病毒构建肾母细胞瘤hsa_circ_0001900稳定过表达细胞株Note： A. Expression of hsa_circ_0001900 is upregulated in Wilms tumor cell lines. B. Fluorescence efficiency of Wilms tumor cell lines infected with lentivirus. C. PCR verification of the overexpression of hsa_circ_0001900 in Wilms tumor cell lines. NC—negative control; OV—overexpression.

Fig 1 Construction of Wilms tumor cell lines with stable overexpression of hsa_circ_0001900 using lentiviral Vectors

图2 基于稳转细胞系的转录组测序和生物信息学分析Note： A. Flowchart of transcriptome sequencing analysis of hsa_circ_0001900-overexpressing and control Wilms tumor cell lines. B. Principal component analysis (PCA) based on gene expression profiles significantly distinguished different cellular phenotypes. C. Volcano plot of differentially expressed genes. D. GO-BP enrichment analysis of differentially expressed gene sets.

Fig 2 Transcriptome sequencing and bioinformatics analyses based on stably transfected cell lines

图3 过表达hsa_circ_0001900在体外促进肾母细胞瘤细胞增殖、迁移和侵袭能力Note： A‒C. CCK-8 assays showed that overexpression of hsa_circ_0001900 significantly promoted the proliferation of WIT-49 (A), WT-CLS1 (B), and SK-NEP-1 (C) cells. D. Wound-healing assays demonstrated that overexpression of hsa_circ_0001900 significantly enhanced the migration ability of WIT-49 cells. E. Transwell assays indicated that overexpression of hsa_circ_0001900 markedly increased the invasive capacity of WIT-49 cells. Bright-field microscopy (×100), scale bar=100 μm. ①P=0.001, compared with the NC group.

Fig 3 Overexpression of hsa_circ_0001900 promotes proliferation, migration, and invasion of Wilms tumor cells in vitro

图4 沉默hsa_circ_0001900抑制肾母细胞瘤细胞的增殖、迁移和侵袭能力Note： A. siRNA-1 exhibited the highest silencing efficiency against hsa_circ_0001900. B－D. CCK-8 assay (B), wound-healing assay (C), and Transwell assay (D) demonstrated that silencing hsa_circ_0001900 significantly suppressed the proliferation, migration, and invasion of WIT-49 cells. Bright-field microscopy (×100), scale bar=100 μm.

Fig 4 Silencing hsa_circ_0001900 inhibits the proliferation, migration, and invasion of Wilms tumor cells

图5 沉默hsa_circ_0001900诱导肾母细胞瘤WIT-49细胞凋亡Note： A. Apoptosis was detected by TUNEL assay. B. Apoptosis was determined by flow cytometry.

Fig 5 Silencing hsa_circ_0001900 induces apoptosis in WIT-49 Wilms tumor cells

图6 hsa_circ_0001900相关转录组测序GSEA、GSVA及关键机制预测Note： A/B. GSEA (A) and GSVA (B) analyses of hsa_circ_0001900 based on transcriptomic sequencing data. C. The cell cycle pathway may be a key mechanism underlying the biological functions of hsa_circ_0001900. TCA—tricarboxylic acid; TGF-β—transforming growth factor-β; PI3K—phosphatidylinositol 3-kinase; Akt—protein kinase B; MAPK—mitogen-activated protein kinase; cAMP—cyclic adenosine monophosphate; JAK—Janus kinase; STAT—signal transducer and activator of transcription; mTOR—mechanistic target of rapamycin; Rap1—Ras-association proximate 1; AMPK—AMP-activated protein kinase; HIF-1—hypoxia-inducible factor 1; NF-κB—nuclear factor-κB; TNF—tumor necrosis factor; IL-17—interleukin-17; VEGF—vascular endothelial growth factor; PPAR—peroxisome proliferator-activated receptor; GnRH—Gonadotropin-releasing hormone; RIG-Ⅰ—retinoic acid-inducible gene Ⅰ.

Fig 6 GSEA, GSVA, and key mechanism prediction of hsa_circ_0001900 based on transcriptome sequencing

图7 hsa_circ_0001900通过促进G1/S期转换调节肾母细胞瘤细胞周期通路Note： A‒C. Flow cytometric analysis of the cell cycle showed that overexpression of hsa_circ_0001900 shortened the G1 phase and prolonged the S phase in WIT-49 (A), WT-CLS1 (B), and SK-NEP-1 (C) cells.

Fig 7 hsa_circ_0001900 regulates the cell cycle pathway in Wilms tumor cells by promoting G1/S phase transition

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hsa_circ_0001900通过加速G1/S细胞周期转换促进肾母细胞瘤细胞增殖、迁移、侵袭并抑制其凋亡

hsa_circ_0001900 enhances the proliferation, migration, and invasion of Wilms tumor cells while suppressing apoptosis through acceleration of G1/S cell cycle transition

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