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FKBP10 promotes proliferation of glioma cells via activating AKT-CREB-PCNA axis.


ABSTRACT:

Background

Although the availability of therapeutic options including temozolomide, radiotherapy and some target agents following neurosurgery, the prognosis of glioma patients remains poor. Thus, there is an urgent need to explore possible targets for clinical treatment of this disease.

Methods

Tissue microarrays and immunohistochemistry were used to detect FKBP10, Hsp47, p-AKT (Ser473), p-CREB (Ser133) and PCNA expression in glioma tissues and xenografts. CCK-8 tests, colony formation assays and xenograft model were performed to test proliferation ability of FKBP10 in glioma cells in vitro and in vivo. Quantitative reverse transcriptase-PCR, western-blotting, GST-pull down, co-immunoprecipitation and confocal-immunofluorescence staining assay were used to explore the molecular mechanism underlying the functions of overexpressed FKBP10 in glioma cells.

Results

FKBP10 was highly expressed in glioma tissues and its expression was positively correlates with grade, poor prognosis. FKBP10-knockdown suppressed glioma cell proliferation in vitro and subcutaneous/orthotopic xenograft tumor growth in vivo. Silencing of FKBP10 reduced p-AKT (Ser473), p-CREB (Ser133), PCNA mRNA and PCNA protein expression in glioma cells. FKBP10 interacting with Hsp47 enhanced the proliferation ability of glioma cells via AKT-CREB-PCNA cascade. In addition, correlation between these molecules were also found in xenograft tumor and glioma tissues.

Conclusions

We showed for the first time that FKBP10 is overexpressed in glioma and involved in proliferation of glioma cells by interacting with Hsp47 and activating AKT-CREB-PCNA signaling pathways. Our findings suggest that inhibition of FKBP10 related signaling might offer a potential therapeutic option for glioma patients.

SUBMITTER: Cai HQ 

PROVIDER: S-EPMC7871608 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature

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Publications

FKBP10 promotes proliferation of glioma cells via activating AKT-CREB-PCNA axis.

Cai Hong-Qing HQ   Zhang Min-Jie MJ   Cheng Zhi-Jian ZJ   Yu Jing J   Yuan Qing Q   Zhang Jin J   Cai Yan Y   Yang Li-Yan LY   Zhang Yu Y   Hao Jia-Jie JJ   Wang Ming-Rong MR   Wan Jing-Hai JH  

Journal of biomedical science 20210209 1


<h4>Background</h4>Although the availability of therapeutic options including temozolomide, radiotherapy and some target agents following neurosurgery, the prognosis of glioma patients remains poor. Thus, there is an urgent need to explore possible targets for clinical treatment of this disease.<h4>Methods</h4>Tissue microarrays and immunohistochemistry were used to detect FKBP10, Hsp47, p-AKT (Ser473), p-CREB (Ser133) and PCNA expression in glioma tissues and xenografts. CCK-8 tests, colony for  ...[more]

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