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Updated: Aug 2, 2025

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
Circular RNA XRCC5 aggravates glioma progression by activating CLC3/SGK1 axis via recruiting IGF2BP2
Li-Ming Tan1, Ping Chen1, Zhen-Yu Nie1
1Department of Neurosurgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan Province, PR China.
Background:
Increasing evidences have reported the critical roles of circular RNA (circRNA) in gliomas. Whereas, the role of circXRCC5 in glioma and its underlying molecular mechanism has not been reported.
Methods:
The RNA transcripts and protein levels were detected using qRT-PCR, immunohistochemistry (IHC) and in situ hybridization (ISH) assays. Cell proliferation was characterized by CCK-8 and clone formation assays. The formation of NLRP3-inflammasomes was identified using immunofluorescence (IF) and Western blot assays. The cytokines were determined using immunosorbent assay (ELISA) and Western blot assays. The molecular interactions were validated using RIP and pull-down assays.
Results:
circXRCC5 was over-expressed in glioma and positively related to the shorter survival rate, advanced TNM stage and larger tumor volume. circXRCC5 knockdown inhibited cell proliferation and NLRP3-mediated inflammasome activation of glioma cells. Subsequently, we found that circXRCC5 maintained mRNA stability of CLC3 by binding to IGF2BP2. Furthermore, CLC3 accelerated SGK1 expression via PI3K/PDK1/AKT pathway. The rescue experiments showed that both overexpression of CLC3 or SGK1 dramatically alleviated circXRCC5 knockdown-induced inhibition of cell proliferation and NLRP3-mediated inflammasome activation of glioma cells. In vivo, our study proved that circXRCC5 accelerated glioma growth by regulating CLC3/SGK1 axis.
Conclusion:
Our data concluded that circXRCC5 formed a complex with IGF2BP2 to regulate inflammasome activation and tumor growth via CLC3/SGK1 axis.
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