Emerging Cellular Therapies for Glioblastoma Multiforme

Choi, Paul J; Tubbs, RR; Oskouian, Rod J.

doi:10.7759/cureus.2305

Cited by 5 publications

(2 citation statements)

References 8 publications

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“…Specially, characterized by its high heterogeneous, widespread consistent infiltration, quick malignant progression. Despite effective treatments including surgical removal, chemotherapy and radiotherapy delay the development and progression to some extent [26][27][28]. Its current clinical prognosis remains badly poor.…”

Section: Discussionmentioning

confidence: 99%

Effect of p21-activated kinase 1 inhibition on proliferation, migration and invasion of glioma

Yi¹,

Chen²,

Zhou³

et al. 2020

Preprint

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Background: Abnormally expressed the p21-activated kinases (PAKs) are implicated in the development and treatment of glioma. Previous study has reported that PAK1 is expressed in glioma. However, the role and mechanism of PAK1 in glioma progression remain unclear.Methods: Western blotting was employed to detect the expression of PAK1 in human glioma tissues. CCK-8, EdU and colony formation assay were applied to evaluate the effect of PAK1 inhibition on cell proliferation of glioma. The flow cytometry was utilized to examine the cell cycle distribution and apoptotic rate of glioma. Wound healing and transwell assay were exploited to investigate the effect of PAK1 inhibition on cell migration and invasion of glioma. The orthotopic xenograft glioma model was established to probe the effect of PAK1 silencing on tumor formation of U87 cell. Results: It was showed that PAK1 was significantly upregulated in glioma tissues. Besides, high level of PAK1 was found to be associated with poor prognosis in glioma patients in TCGA database. PAK1 inhibition restrained cell proliferation, arrested cells at G1 phase, and induced cell apoptosis of glioma. PAK1 inhibition suppressed glioma cell migration and invasion. Moreover, knockdown of PAK1 dramatically decreased the protein expressions including MDM2, p38, p-p38, CyclinD1, CDK4, Bcl-2, MMP2, MMP9, Cofilin, while increased the protein levels of p53, Bax, p21 and Cleaved Caspase-3. Finally, orthotopic xenograft glioma model confirmed that silencing of PAK1 repressed the tumor formation of U87 cell transplantation.Conclusion: Our study described that PAK1 inhibition impedes proliferation, migration and invasion of glioma cells and thus probably as a novel target for glioma therapy.

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Section: Discussionmentioning

confidence: 99%

Effect of p21-activated kinase 1 inhibition on proliferation, migration and invasion of glioma

Yi¹,

Chen²,

Zhou³

et al. 2020

Preprint

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“…3,4 While great effort has been put towards understanding how glioblastoma develop and progress the molecular mechanisms governing these processes remain to be fully clarifie. 5,6 Tousled-like kinases (TLKs) are a family of serine/threonine kinases located in the nucleus that promote S-phase chromatin assembly and mitotic chromosome segregatio. 7,8 There are two genes in the TLK family-TLK1 and TLK.…”

Section: Introductionmentioning

confidence: 99%

TLK2 enhances aggressive phenotypes of glioblastoma cells through the activation of SRC signaling pathway

Lin

Yao

Zhao

et al. 2018

Cancer Biology & Therapy

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Glioblastoma are among the most common forms of cancer affecting the central nervous system, and yet there is currently no effective means of treating them. In the current study, we reported that tousled-like kinase 2 (TLK2) is a key factor in glioblastoma that modulates SRC signaling, thereby driving tumor malignancy. TLK2 is commonly upregulated in glioblastoma, and such upregulation was associated with poor patient outcomes. TLK2 overexpression induced cell growth, migration, invasion, and epithelial-mesenchymal transition, and cell cycle arrest, while TLK2 knockdown had the opposite effect. SRC pathway inhibition by Saracatinib resulted in reduced TLK2-mediated glioblastoma migration, invasion, confirming a key role for SRC signaling in regulating the functions of TLK2. Together, our findings demonstrate that glioblastoma TLK2 overexpression acts as a key driver of tumor malignancy via SRC signaling pathway.

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Inhibitory effects of temozolomide on glioma cells is sensitized by RSL3-induced ferroptosis but negatively correlated with expression of ferritin heavy chain 1 and ferritin light chain

Yang

Wang

Zhu

et al. 2022

Laboratory Investigation

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Emerging Cellular Therapies for Glioblastoma Multiforme

Cited by 5 publications

References 8 publications

Effect of p21-activated kinase 1 inhibition on proliferation, migration and invasion of glioma

Effect of p21-activated kinase 1 inhibition on proliferation, migration and invasion of glioma

TLK2 enhances aggressive phenotypes of glioblastoma cells through the activation of SRC signaling pathway

Inhibitory effects of temozolomide on glioma cells is sensitized by RSL3-induced ferroptosis but negatively correlated with expression of ferritin heavy chain 1 and ferritin light chain

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