Regulation of glioblastoma cell invasion by PKCι and RhoB

Baldwin, R. Mitchell; Parolin, Doris A. E.; Lorimer, Ian A. J.

doi:10.1038/sj.onc.1211027

Cited by 56 publications

(56 citation statements)

References 35 publications

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“…It participates in diverse cellular process including actin organization, differentiation to block cell migration activity. Introduction of exogenous RhoB suppresses glioma cell mobility and invasiveness by reducing activation of PKC iota and PKB/AKT 48. MiR‐19 is reported to promote glioma cell invasion and migration by directly suppressing RhoB by miR‐19 25.…”

Section: Mir‐19 In Gliomamentioning

confidence: 99%

The emerging role of miR‐19 in glioma

Wang

Zhang

Hao

et al. 2018

J Cellular Molecular Medi

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Glioma has been regarded as the most common, highly proliferative and invasive brain tumour. Advances in research of miRNAs in glioma are toward further understanding of the pathogenesis of glioma. MiR‐19, a member of miR‐17~92 cluster, was reported to play an oncogenic role in tumourigenesis. Here we review the identified data about the effect of miR‐19 on proliferation, apoptosis, migration and invasion of glioma cells, the target genes regulated by miR‐19, and correlation of miR‐19 with the sensitivity of glioma cells to chemotherapy and radiotherapy. It is concluded that miR‐19 plays an important role in the pathogenesis of glioma and can be a potential target for gene therapy of glioma.

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Section: Mir‐19 In Gliomamentioning

confidence: 99%

The emerging role of miR‐19 in glioma

Wang

Zhang

Hao

et al. 2018

J Cellular Molecular Medi

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“…In these cells, PKCi is activated by loss of PTEN rather than by PIK3CA mutation (Baldwin et al, 2008).…”

Section: Pkci Represses Senescence In Glioblastomamentioning

confidence: 99%

“…It is overexpressed in multiple cancer types, and studies of both mouse models and human cancer cell lines show an important role in the growth, invasion and resistance to apoptosis of a variety of cancer cell types. In glioblastoma, PKCi represses apoptosis and promotes invasion (Baldwin et al, 2006(Baldwin et al, , 2008. PKCi also has a key role in the pathogenesis of lung, ovarian and pancreatic cancer (Eder et al, 2005;Regala et al, 2005;Zhang et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Repression of cancer cell senescence by PKCι

et al. 2011

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“…A synergistic effect of TAM with radiation in C6 glioma cells has been demonstrated, and may partially be due to the inhibition of PKC activation (18). The atypical PKC family member, PKC-ι was of particular interest as it is a key regulator of cell survival, proliferation, invasion and chemoresistance in glioma (27,30,34,35). The present results revealed an inhibitory role of TAM in the expression levels of p-PKC-ι, which may participate in the radioresistance of glioma cells.…”

Section: Discussionmentioning

confidence: 99%

Radiosensitization of human glioma cells by tamoxifen is associated with the inhibition of PKC-ι activity in vitro

et al. 2015

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Abstract. The present study aimed to investigate the radiosensitizing effects of tamoxifen (TAM), a non-steroidal anti-estrogen drug, in human glioma A172 and U251 cells in vitro. A colony-forming assay revealed that TAM enhances radiosensitivity in A172 and U251 cells. Treatment with TAM also increased the percentage of apoptotic cells subsequent to ionizing radiation, and increased the expression of apoptotic markers, including cleaved caspase-3 and poly(ADP-ribose) polymerase. Ionizing radiation induced G2/M phase arrest, which was alleviated within 24 h when the radiation-induced DNA damage was repaired. However, flow cytometry analysis revealed that TAM treatment delayed the recovery of cell cycle progression. Additional examination demonstrated that TAM-mediated protein kinase C-ι (PKC-ι) inhibition may lead to the activation of pro-apoptotic B-cell lymphoma 2-associated death promoter, and the dephosphorylation of cyclin-dependent kinase 7, resulting in increased cell apoptosis and sustained G2/M phase arrest following exposure to radiation. The present data indicate that the radiosensitizing effects of TAM on glioma cells are partly due to the inhibition of PKC-ι activity in vitro.

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Regulation of glioblastoma cell invasion by PKCι and RhoB

Cited by 56 publications

References 35 publications

The emerging role of miR‐19 in glioma

The emerging role of miR‐19 in glioma

Repression of cancer cell senescence by PKCι

Radiosensitization of human glioma cells by tamoxifen is associated with the inhibition of PKC-ι activity in vitro

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