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K-RAS Acts as a Critical Regulator of CD44 to Promote the Invasiveness and Stemness of GBM in Response to Ionizing Radiation

Authors
 Yi Zhao  ;  Jae-Hyeok Kang  ;  Ki-Chun Yoo  ;  Seok-Gu Kang  ;  Hae-June Lee  ;  Su-Jae Lee 
Citation
 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, Vol.22(20) : 10923, 2021-10 
Journal Title
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Issue Date
2021-10
MeSH
Brain Neoplasms / metabolism ; Brain Neoplasms / mortality ; Brain Neoplasms / pathology* ; Cell Line, Tumor ; Cell Movement / radiation effects ; Down-Regulation / drug effects ; Extracellular Signal-Regulated MAP Kinases / metabolism ; Glioblastoma / metabolism ; Glioblastoma / mortality ; Glioblastoma / pathology* ; Humans ; Hyaluronan Receptors / antagonists & inhibitors ; Hyaluronan Receptors / genetics ; Hyaluronan Receptors / metabolism* ; Kaplan-Meier Estimate ; MicroRNAs / metabolism ; Proto-Oncogene Proteins p21(ras) / genetics ; Proto-Oncogene Proteins p21(ras) / metabolism* ; RNA Interference ; RNA, Small Interfering / metabolism ; Radiation, Ionizing* ; Signal Transduction / radiation effects*
Keywords
CD44 ; K-RAS ; glioblastoma (GBM) ; ionizing radiation
Abstract
Radiation therapy is a current standard-of-care treatment and is used widely for GBM patients. However, radiation therapy still remains a significant barrier to getting a successful outcome due to the therapeutic resistance and tumor recurrence. Understanding the underlying mechanisms of this resistance and recurrence would provide an efficient approach for improving the therapy for GBM treatment. Here, we identified a regulatory mechanism of CD44 which induces infiltration and mesenchymal shift of GBM. Ionizing radiation (IR)-induced K-RAS/ERK signaling activation elevates CD44 expression through downregulation of miR-202 and miR-185 expression. High expression of CD44 promotes SRC activation to induce cancer stemness and EMT features of GBM cells. In this study, we demonstrate that the K-RAS/ERK/CD44 axis is a key mechanism in regulating mesenchymal shift of GBM cells after irradiation. These findings suggest that blocking the K-RAS activation or CD44 expression could provide an efficient way for GBM treatment.
Files in This Item:
T202105470.pdf Download
DOI
10.3390/ijms222010923
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurosurgery (신경외과학교실) > 1. Journal Papers
Yonsei Authors
Kang, Seok Gu(강석구) ORCID logo https://orcid.org/0000-0001-5676-2037
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/187305
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