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IRTKS 促进宫颈癌细胞的恶性进展。

IRTKS contributes to the malignant progression of cervical cancer cells.

机构信息

Molecular Medicine and Cancer Research Center, Chongqing Medical University, No. 1, Medical College Road, Yuzhong District, Chongqing, China.

Department of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing, China.

出版信息

Med Oncol. 2024 Jun 13;41(7):174. doi: 10.1007/s12032-024-02410-9.

DOI:10.1007/s12032-024-02410-9
PMID:38869721
Abstract

Cervical cancer (CC), one of the most aggressive tumors in women, has high risk rates of recurrence and metastasis. It is essential to study the key genes and proteins involved in CC development. IRTKS, a member of the IRSp53 family, has been reported as a tumor promoter in gastric and breast cancers. However, the biological role of IRTKS in CC is still unclear. The purpose of this study was to explore the biological function of IRTKS in CC cells in vitro and the effect of IRTKS on tumorigenesis in vivo. Siha and Hela cells were treated with si-RNA and plasmids. Cell proliferation and growth were detected by CCK8, colony formation assay and nude mouse tumorigenicity assay, respectively. Transwell assay was used to analyze cell migration and invasion. The expression of epithelial-mesenchymal transition (EMT)-related proteins was determined by western blot. IRTKS was highly expressed in CC. IRTKS contributed to the proliferation of CC cells in vitro and in vivo. Furthermore, IRTKS facilitated the migration and invasion of CC cells and modulated EMT. IRTKS plays a crucial role in CC tumorigenesis, suggesting it may be a potential key gene for new therapeutic strategies in CC.

摘要

宫颈癌 (CC) 是女性中最具侵袭性的肿瘤之一,具有较高的复发和转移风险。研究参与 CC 发展的关键基因和蛋白至关重要。IRTKS 是 IRSp53 家族的成员,已被报道为胃癌和乳腺癌的肿瘤促进因子。然而,IRTKS 在 CC 中的生物学作用尚不清楚。本研究旨在探讨 IRTKS 在体外 CC 细胞中的生物学功能以及 IRTKS 对体内肿瘤发生的影响。使用 siRNA 和质粒处理 Siha 和 Hela 细胞。分别通过 CCK8、集落形成实验和裸鼠肿瘤形成实验检测细胞增殖和生长。通过 Transwell 分析检测细胞迁移和侵袭。通过 Western blot 检测上皮-间充质转化 (EMT) 相关蛋白的表达。IRTKS 在 CC 中高表达。IRTKS 促进了 CC 细胞在体外和体内的增殖。此外,IRTKS 促进了 CC 细胞的迁移和侵袭,并调节了 EMT。IRTKS 在 CC 肿瘤发生中起关键作用,提示它可能是 CC 新治疗策略的潜在关键基因。

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本文引用的文献

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BAIAP2L1 accelerates breast cancer progression and chemoresistance by activating AKT signaling through binding with ribosomal protein L3.BAIAP2L1 通过与核糖体蛋白 L3 结合激活 AKT 信号通路从而促进乳腺癌的进展和化疗耐药性。
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Insulin receptor tyrosine kinase substrate (IRTKS) promotes the tumorigenesis of pancreatic cancer via PI3K/AKT signaling.
胰岛素受体酪氨酸激酶底物 (IRTKS) 通过 PI3K/AKT 信号通路促进胰腺癌的肿瘤发生。
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