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钙/钙调蛋白依赖性蛋白激酶1D通过PI3K/AKT/mTOR信号通路抑制胶质瘤。

CAMK1D Inhibits Glioma Through the PI3K/AKT/mTOR Signaling Pathway.

作者信息

Jin Qianxu, Zhao Jiahui, Zhao Zijun, Zhang Shiyang, Sun Zhimin, Shi Yunpeng, Yan Hongshan, Wang Yizheng, Liu Liping, Zhao Zongmao

机构信息

Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

出版信息

Front Oncol. 2022 Apr 13;12:845036. doi: 10.3389/fonc.2022.845036. eCollection 2022.

DOI:10.3389/fonc.2022.845036
PMID:35494053
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9043760/
Abstract

Calcium/calmodulin-dependent protein ID (CAMK1D) is widely expressed in many tissues and involved in tumor cell growth. However, its role in gliomas has not yet been elucidated. This study aimed to investigate the roles of CAMK1D in the proliferation, migration, and invasion of glioma. Through online datasets, Western blot, and immunohistochemical analysis, glioma tissue has significantly lower CAMK1D expression levels than normal brain (NB) tissues, and CAMK1D expression was positively correlated with the WHO classification. Kaplan-Meier survival analysis shows that CAMK1D can be used as a potential prognostic indicator to predict the overall survival of glioma patients. In addition, colony formation assay, cell counting Kit-8, and xenograft experiment identified that knockdown of CAMK1D promotes the proliferation of glioma cells. Transwell and wound healing assays identified that knockdown of CAMK1D promoted the invasion and migration of glioma cells. In the above experiments, the results of overexpression of CAMK1D were all contrary to those of knockdown. In terms of mechanism, this study found that CAMK1D regulates the function of glioma cells by the PI3K/AKT/mTOR pathway. In conclusion, these findings suggest that CAMK1D serves as a prognostic predictor and a new target for developing therapeutics to treat glioma.

摘要

钙/钙调蛋白依赖性蛋白激酶1D（CAMK1D）在许多组织中广泛表达，并参与肿瘤细胞生长。然而，其在胶质瘤中的作用尚未阐明。本研究旨在探讨CAMK1D在胶质瘤增殖、迁移和侵袭中的作用。通过在线数据集、蛋白质印迹法和免疫组织化学分析，发现胶质瘤组织中CAMK1D表达水平显著低于正常脑组织（NB），且CAMK1D表达与世界卫生组织（WHO）分级呈正相关。Kaplan-Meier生存分析表明，CAMK1D可作为预测胶质瘤患者总生存的潜在预后指标。此外，集落形成实验、细胞计数试剂盒-8（CCK-8）实验和异种移植实验表明，敲低CAMK1D可促进胶质瘤细胞增殖。Transwell实验和伤口愈合实验表明，敲低CAMK1D可促进胶质瘤细胞侵袭和迁移。在上述实验中，CAMK1D过表达的结果均与敲低结果相反。机制方面，本研究发现CAMK1D通过PI3K/AKT/mTOR信号通路调节胶质瘤细胞功能。总之，这些发现表明CAMK1D可作为一种预后预测指标，也是开发治疗胶质瘤新疗法的一个新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9705/9043760/95cbd4a5be6e/fonc-12-845036-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9705/9043760/95cbd4a5be6e/fonc-12-845036-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9705/9043760/6f733807163e/fonc-12-845036-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9705/9043760/b8cc75ebdc32/fonc-12-845036-g002.jpg
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