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

被引：9
作者：
Jin, Qianxu [1 ]
Zhao, Jiahui [2 ]
Zhao, Zijun [1 ]
Zhang, Shiyang [1 ]
Sun, Zhimin [3 ]
Shi, Yunpeng [1 ]
Yan, Hongshan [1 ]
Wang, Yizheng [1 ]
Liu, Liping [2 ]
Zhao, Zongmao [1 ]
机构：
[1] Hebei Med Univ, Dept Neurosurg, Hosp 2, Shijiazhuang, Hebei, Peoples R China
[2] Capital Med Univ, Beijing Tiantan Hosp, Dept Neurol, Beijing, Peoples R China
[3] Third Hosp Shijiazhuang City, Dept Neurosurg, Shijiazhuang, Hebei, Peoples R China
来源：
FRONTIERS IN ONCOLOGY | 2022年 / 12卷
基金：
中国国家自然科学基金;
关键词：
CAMK1D; glioma; cell proliferation; prognosis; PI3K; AKT; mTOR; PROTEIN-KINASE-I; GROWTH; EXPRESSION; CANCER; ROLES; CELLS; CKLIK; CYCLE;
D O I：
10.3389/fonc.2022.845036
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
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.
引用
收藏
页数：12
相关论文
共 35 条
[1]   CAMK1D amplification implicated in epithelial-mesenchymal transition in basal-like breast cancer [J].
Bergamaschi, Anna ;
Kim, Young H. ;
Kwei, Kevin A. ;
Choi, Yoon La ;
Bocanegra, Melanie ;
Langerod, Anita ;
Han, Wonshik ;
Noh, Dony-Young ;
Huntsman, David G. ;
Jeffrey, Stefanie S. ;
Borresen-Dale, Anne-Lise ;
Pollack, Jonathan R. .
MOLECULAR ONCOLOGY, 2008, 2 (04) :327-339
[2]   Intranasal Perillyl Alcohol for Glioma Therapy: Molecular Mechanisms and Clinical Development [J].
Chen, Thomas C. ;
da Fonseca, Clovis O. ;
Schonthal, Axel H. .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2018, 19 (12)
[3]   Calmodulin-dependent kinase I regulates adrenal cell expression of aldosterone synthase [J].
Condon, JC ;
Pezzi, V ;
Drummond, BM ;
Yin, S ;
Rainey, WE .
ENDOCRINOLOGY, 2002, 143 (09) :3651-3657
[4]   Role of the PI3K/AKT/mTOR signaling pathway in ovarian cancer: Biological and therapeutic significance [J].
Ediriweera, Meran Keshawa ;
Tennekoon, Kamani Hemamala ;
Samarakoon, Sameera Ranganath .
SEMINARS IN CANCER BIOLOGY, 2019, 59 :147-160
[5]   Citrate activates autophagic death of prostate cancer cells via downregulation CaMKII/AKT/mTOR pathway [J].
Fan, Xirui ;
Zhou, Jinyi ;
Yan, Xintong ;
Bi, Xiaowen ;
Liang, Juanjuan ;
Lu, Shuai ;
Luo, Lan ;
Zhou, Da ;
Yin, Zhimin .
LIFE SCIENCES, 2021, 275
[6]   MiR-137 inhibits the proliferation, invasion and migration of glioma via targeting to regulate EZH2 [J].
Gu, Jingshun ;
Wang, Juntong ;
You, Aiwu ;
Li, Jun ;
Zhang, Yuyan ;
Rao, Guomin ;
Ge, Xuehua ;
Zhang, Kun ;
Liu, Xuan ;
Wang, Dongchun .
GENES & GENOMICS, 2021, 43 (10) :1157-1165
[7]   Glioma epigenetics: From subclassification to novel treatment options [J].
Gusyatiner, Olga ;
Hegi, Monika E. .
SEMINARS IN CANCER BIOLOGY, 2018, 51 :50-58
[8]  
Jusuf AA., 2015, KOBE J MED SCI, V61, P115
[9]   Spatiotemporal expression of four isoforms of Ca2+/calmodulin-dependent protein kinase I in brain and its possible roles in hippocampal dendritic growth [J].
Kamata, Akifumi ;
Sakagami, Hiroyuki ;
Tokumitsu, Hiroshi ;
Owada, Yuji ;
Fukunaga, Kohji ;
Kondo, Hisatake .
NEUROSCIENCE RESEARCH, 2007, 57 (01) :86-97
[10]   mTOR Signaling in Growth Control and Disease [J].
Laplante, Mathieu ;
Sabatini, David M. .
CELL, 2012, 149 (02) :274-293
1234