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CDCA3通过激活Akt/mTOR信号通路促进下咽鳞状细胞癌细胞的增殖和迁移。

CDCA3 promotes the proliferation and migration of hypopharyngeal squamous cell carcinoma cells by activating the Akt/mTOR pathway.

作者信息

Wu Junfu, Cui Meng, Wang Jiheng, Fan Jie, Liu Shanting, Lou Weihua

机构信息

Department of Head Neck and Thyroid Surgery, the Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, Zhengzhou, Henan, China.

Department of Otolaryngology-Head and Neck Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

出版信息

Biotechnol Genet Eng Rev. 2024 Oct;40(2):707-725. doi: 10.1080/02648725.2023.2187876. Epub 2023 Mar 9.

DOI:10.1080/02648725.2023.2187876
PMID:36892980
Abstract

Hypopharyngeal squamous cell carcinoma (HSCC) is a highly invasive and fatal tumor with a poor prognosis in head and neck tumors. It is urgent to further study the molecular mechanism of HSCC progression and identify new effective therapeutic targets. Cell division cycle-related protein 3 (CDCA3) was reported overexpressed in several cancers and involved in tumor progression. However, the biological role of CDCA3 and its potential mechanism in HSCC remain undetermined. Reverse transcription quantitative polymerase chain reaction (RT-PCR) and immunohistochemistry were used to detect the expression levels of CDCA3 in HSCC tissue and matched peritumoral tissue. The effects of CDCA3 on cell proliferation, invasion, and migration were explored using the Celigo image cytometry assay, MTT assay, flow cytometric analysis, cell invasion, and migration assays. The results showed that CDCA3 was upregulated in HSCC tissue and FaDu cell line. Knockdown of CDCA3 inhibited the proliferation, invasion, and migration of FaDu cells and promoted apoptosis of FaDu cells. Furthermore, knockdown of CDCA3 blocked the cell cycle in the G0/G1 phase. Mechanistically, CDCA3 may play a role in tumor progression of HSCC through the Akt/mTOR signaling pathway. In summary, these results suggest that CDCA3 serves as an oncogene in HSCC and may be used as a prognostic indicator and a potential therapeutic target for HSCC.

摘要

下咽鳞状细胞癌(HSCC)是一种侵袭性很强且致命的肿瘤,在头颈部肿瘤中预后较差。进一步研究HSCC进展的分子机制并确定新的有效治疗靶点迫在眉睫。据报道,细胞分裂周期相关蛋白3(CDCA3)在几种癌症中过表达,并参与肿瘤进展。然而,CDCA3在HSCC中的生物学作用及其潜在机制仍未明确。采用逆转录定量聚合酶链反应(RT-PCR)和免疫组织化学法检测HSCC组织及癌旁组织中CDCA3的表达水平。使用Celigo图像细胞术检测、MTT检测、流式细胞术分析、细胞侵袭和迁移检测等方法,探讨CDCA3对细胞增殖、侵袭和迁移的影响。结果显示,CDCA3在HSCC组织和FaDu细胞系中上调。敲低CDCA3可抑制FaDu细胞的增殖、侵袭和迁移,并促进FaDu细胞凋亡。此外,敲低CDCA3可使细胞周期阻滞在G0/G1期。机制上,CDCA3可能通过Akt/mTOR信号通路在HSCC的肿瘤进展中发挥作用。总之,这些结果表明CDCA3在HSCC中作为癌基因发挥作用,可能作为HSCC的预后指标和潜在治疗靶点。

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