KIS, a target of SOX4, regulates the ID1-mediated enhancement of β-catenin to facilitate lung adenocarcinoma cell proliferation and metastasis.

IF 2.7 3区医学 Q3 ONCOLOGY

Journal of Cancer Research and Clinical Oncology Pub Date : 2024-07-25 DOI:10.1007/s00432-024-05853-9

Jing-Xia Chang, Meng Zhang, Li-Li Lou, He-Ying Chu, Hua-Qi Wang

{"title":"KIS, a target of SOX4, regulates the ID1-mediated enhancement of β-catenin to facilitate lung adenocarcinoma cell proliferation and metastasis.","authors":"Jing-Xia Chang, Meng Zhang, Li-Li Lou, He-Ying Chu, Hua-Qi Wang","doi":"10.1007/s00432-024-05853-9","DOIUrl":null,"url":null,"abstract":"Purpose: Kinase interacting with stathmin (KIS) is a serine/threonine kinase involved in RNA processing and protein phosphorylation. Increasing evidence has suggested its involvement in cancer progression. The aim of this study was to investigate the role of KIS in the development of lung adenocarcinoma (LUAD). Dual luciferase assay was used to explore the relationship between KIS and SOX4, and its effect on ID1/β-catenin pathway.Methods: Real-time qPCR and western blot were used to assess the levels of KIS and other factors. Cell proliferation, migration, and invasion were monitored, and xenograft animal model were established to investigate the biological functions of KIS in vitro and in vivo.Results: In the present study, KIS was found to be highly expressed in LUAD tissues and cell lines. KIS accelerated the proliferative, migratory and invasive abilities of LUAD cells in vitro, and promoted the growth of LUAD in a mouse tumor xenograft model in vivo. Mechanistically, KIS activated the β-catenin signaling pathway by modulating the inhibitor of DNA binding 1 (ID1) and was transcriptionally regulated by SOX4 in LUAD cells.Conclusion: KIS, a target of SOX4, regulates the ID1-mediated enhancement of β-catenin to facilitate LUAD cell invasion and metastasis.","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11272720/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cancer Research and Clinical Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00432-024-05853-9","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Purpose: Kinase interacting with stathmin (KIS) is a serine/threonine kinase involved in RNA processing and protein phosphorylation. Increasing evidence has suggested its involvement in cancer progression. The aim of this study was to investigate the role of KIS in the development of lung adenocarcinoma (LUAD). Dual luciferase assay was used to explore the relationship between KIS and SOX4, and its effect on ID1/β-catenin pathway.

Methods: Real-time qPCR and western blot were used to assess the levels of KIS and other factors. Cell proliferation, migration, and invasion were monitored, and xenograft animal model were established to investigate the biological functions of KIS in vitro and in vivo.

Results: In the present study, KIS was found to be highly expressed in LUAD tissues and cell lines. KIS accelerated the proliferative, migratory and invasive abilities of LUAD cells in vitro, and promoted the growth of LUAD in a mouse tumor xenograft model in vivo. Mechanistically, KIS activated the β-catenin signaling pathway by modulating the inhibitor of DNA binding 1 (ID1) and was transcriptionally regulated by SOX4 in LUAD cells.

Conclusion: KIS, a target of SOX4, regulates the ID1-mediated enhancement of β-catenin to facilitate LUAD cell invasion and metastasis.

Abstract Image

查看原文本刊更多论文

KIS是SOX4的靶标，它调节ID1介导的β-catenin增强，从而促进肺腺癌细胞的增殖和转移。

目的：与 stathmin 相互作用的激酶（KIS）是一种丝氨酸/苏氨酸激酶，参与 RNA 处理和蛋白质磷酸化。越来越多的证据表明，它参与了癌症的进展。本研究旨在探讨 KIS 在肺腺癌（LUAD）发展过程中的作用。采用双荧光素酶检测法探讨KIS与SOX4之间的关系及其对ID1/β-catenin通路的影响：方法：采用实时 qPCR 和 Western 印迹法评估 KIS 及其他因子的水平。方法：采用实时 qPCR 和 Western blot 检测 KIS 及其他因子的水平，监测细胞增殖、迁移和侵袭，并建立异种移植动物模型，研究 KIS 在体外和体内的生物学功能：结果：本研究发现，KIS在LUAD组织和细胞系中高表达。结果：本研究发现 KIS 在 LUAD 组织和细胞系中高表达，KIS 在体外可加速 LUAD 细胞的增殖、迁移和侵袭能力，在体内可促进 LUAD 在小鼠肿瘤异种移植模型中的生长。从机理上讲，KIS通过调节DNA结合抑制因子1（ID1）激活了β-catenin信号通路，并在LUAD细胞中受SOX4的转录调控：结论：KIS是SOX4的靶标，可调节ID1介导的β-catenin增强，从而促进LUAD细胞的侵袭和转移。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Journal of Cancer Research and Clinical Oncology 医学-肿瘤学

CiteScore

4.00

自引率

2.80%

发文量

577

审稿时长

2 months

期刊介绍： The "Journal of Cancer Research and Clinical Oncology" publishes significant and up-to-date articles within the fields of experimental and clinical oncology. The journal, which is chiefly devoted to Original papers, also includes Reviews as well as Editorials and Guest editorials on current, controversial topics. The section Letters to the editors provides a forum for a rapid exchange of comments and information concerning previously published papers and topics of current interest. Meeting reports provide current information on the latest results presented at important congresses. The following fields are covered: carcinogenesis - etiology, mechanisms; molecular biology; recent developments in tumor therapy; general diagnosis; laboratory diagnosis; diagnostic and experimental pathology; oncologic surgery; and epidemiology.