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KRT5
JOURNAL OF CLINICAL LABORATORY ANALYSIS · 2022 ·Vol. 36 ·期 4 ·e24347 · IF 3.124

Hsa_circRNA_0017620 regulated cell progression of non-small-cell lung cancer via miR-520a-5p/KRT5 axis

Shan Chen,Kelin Hong,Long Zhou,Ruizhi Ran,Jinqi Huang,Yong Zheng,Maohui Xing,Yanli Cai

Background CircRNA is a very important functional RNA that plays an important role in the development and metabolism of cancer. However, the study of circRNA in NSCLC has not been fully elucidated. Methods The expression of hsa_circ_0017620, SFMBT2, miR-520a-5p, and KRT5 was determined using qRT-PCR. KRT5, Twist1, E-cadherin, and Ki67 protein expression were measured with western blot. The positive expression rates of Ki67 and Vimentin were determined by immunohistochemistry assay. 5-Ethynyl-2’-deoxyuridine (EdU), colony formation, and MTT assays were used to assess cell proliferation. Transwell migration and invasion assay were applied to determine cell migration and invasion. Dual-luciferase reporter and RNA immunoprecipitation assays were used to verify the relationship among hsa_circ_0017620, miR-520a-5p, and KRT5. The animal experiment was used to ensure the effects of hsa_circ_0017620 on tumor growth in vivo . Results Hsa_circ_0017620 was upregulated in NSCLC cells and tissues. MiR-520a-5p had been verified to be a target miRNA of hsa_circ_0017620 and KRT5 had been verified to be a target mRNA of miR-520a-5p in NSCLC cells. Knockdown of hsa_circ_0017620 inhibited cell proliferation, migration, and invasion in NSCLC cells, which was reversed by downregulating miR-520a-5p or upregulating KRT5 in NSCLC. Overexpression of hsa_circ_0017620 had opposite effects in NSCLC. Moreover, hsa_circ_0017620 silencing inhibited tumor growth in vivo of NSCLC. Conclusion In this study, we found that hsa_circ_0017620 played an important role in NSCLC progression. Hsa_circ_0017620 regulated cell proliferation, invasion, and migration through targeting miR-520a-5p/KRT5 axis in NSCLC, providing a potential new target for the treatment and diagnosis of NSCLC.

CAS / MDL: 50-00-0
研究领域: 肿瘤学 · 分子生物学 · 细胞生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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EUROPEAN JOURNAL OF CELL BIOLOGY · 2026 ·Vol. 105 ·期 3 ·151555 · IF 4.3

Spatiotemporal dynamics of epididymal epithelial cells uncover a novel KRT5⁺ATP6V1A⁺ subpopulation of basal cell in postnatal mouse development

Huixia Li,Taoran Xie,David YLChan,Ellis Kin Lam Fok,Liandong Zuo,Gangcai Xie,Qianqian Sha,Hao Chen

Epididymal epithelial cells are critical for sperm maturation. Although previous studies have determined the development of epididymal epithelial cells in rat epididymis, the postnatal developmental trajectories of distinct epithelial cell types in the mouse epididymis remain elusive. Here, we examined the developmental timeline of mouse epididymal epithelium differed from that of the rat by confocal immunostaining and single-cell RNA sequencing (scRNA-seq). In mice, principal and basal cells appeared as early as postnatal day 7 (PD7) across all segments, labeled by AQP9 and KRT5, in contrast to the later emergence in rats (e.g., basal cells at PD14 in rat cauda). ATP6V1A-positive clear cells were detected at PD28 in caput, corpus, and cauda but not in the initial segment, while narrow cells were observed in all segments beginning at PD14. These contrasted with the rat, in which clear cells appeared at PD14. Notably, scRNA-seq and immunostaining identified a previously unrecognized KRT5⁺/ATP6V1A⁺ narrow-like basal cell subpopulation, enriched in lysosomes and mainly localized to the caput and corpus. These findings revealed an earlier epithelial maturation in mice compared to rats, underscoring the importance of choosing animal models. The newly identified basal subpopulation may contribute to luminal acidification and homeostasis, offering new insights into epididymal physiology and reproductive biology.

CAS / MDL: 9005-64-5
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American Journal of Cancer Research · 2024 · IF 3.6

KIF2C is a critical regulator for malignant progression of head and neck squamous cell carcinoma

Haiyue Zhu,Yuxin Bao,Xuanqi Dou,Xiaofeng Zuo,Junhong Ye,Haiyu Ma,Youquan Bu,Yitao Wang,Jiang Zhu

Head and neck squamous cell carcinoma (HNSCC) is a significant cause of mortality, while the underlying mechanism remains unclear. Our studies have revealed that KIF2C plays a crucial role in tumor proliferation and metastasis in HNSCC. The results demonstrate that KIF2C is highly expressed at both the mRNA and protein levels and is closely associated with lymph node metastasis. The gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses indicate that the differentially expressed genes are enriched in processes or pathways related to cell adhesion and cell mitosis in HNSCC. Moreover, the established protein-protein interaction network identifies KIF2C as a potential hub gene in HNSCC. Knockdown of KIF2C has been demonstrated to significantly reduce cell migration and invasion ability, leading to cell cycle arrest, a high proportion of abnormal cell apoptosis, and cell chromosome division mismatches in the HNSCC cell line. Downstream genes such as PDGFA, EGFR, TP63, SNAI2, KRT5, and KRT14 were found to be down-regulated, and multiple critical pathways, including mTOR, ERK, and PI3K-AKT pathways, were inactivated as a result of KIF2C knockdown. These findings provide strong evidence for the crucial role of KIF2C in HNSCC and suggest that targeting KIF2C may be a promising therapeutic strategy for this disease. Knockdown of KIF2C has been shown to significantly inhibit tumor proliferation in nude mice, demonstrating the potential therapeutic role of KIF2C in HNSCC treatment.

CAS / MDL: 33069-62-4
研究领域: 肿瘤学 · 分子生物学 · 细胞生物学 · 癌症研究
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