JNK contributes to temozolomide resistance of stem-like glioblastoma cells via regulation of MGMT expression.

@article{Okada2014JNKCT,
  title={JNK contributes to temozolomide resistance of stem-like glioblastoma cells via regulation of MGMT expression.},
  author={Masashi Okada and Atsushi Sato and Keita Shibuya and Eriko Watanabe and Shizuka Seino and Shuhei Suzuki and Manabu Seino and Yoshitaka Narita and Soichiro Shibui and Takamasa Kayama and Chifumi Kitanaka},
  journal={International journal of oncology},
  year={2014},
  volume={44 2},
  pages={
          591-9
        }
}
While elimination of the cancer stem cell population is increasingly recognized as a key to successful treatment of cancer, the high resistance of cancer stem cells to conventional chemoradiotherapy remains a therapeutic challenge. O6-methylguanine DNA methyltransferase (MGMT), which is frequently expressed in cancer stem cells of glioblastoma, has been implicated in their resistance to temozolomide, the first-line chemotherapeutic agent against newly diagnosed glioblastoma. However, much… 
Potential Strategies Overcoming the Temozolomide Resistance for Glioblastoma
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The current knowledge of different resistance mechanisms, novel strategies for enhancing the effect of TMZ, and emerging therapeutic approaches to eliminate GSCs are summarized with the aim of producing a successful GBM treatment and future directions for basic and clinical research are discussed.
Inhibition of JNK potentiates temozolomide-induced cytotoxicity in U87MG glioblastoma cells via suppression of Akt phosphorylation.
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Hedgehog/Gli1 signaling pathway regulates MGMT expression and chemoresistance to temozolomide in human glioblastoma
TLDR
The in vivo study revealed a synergistic effect on tumor growth inhibition with the combined administration of cyclopamine and TMZ and showed that HH/Gli1 signaling pathway regulates MGMT expression and chemoresistance to TMZ in human GBM independent from MGMT promoter methylation status.
Rho-Associated Protein Kinase (ROCK) Inhibitors Inhibit Survivin Expression and Sensitize Pancreatic Cancer Stem Cells to Gemcitabine.
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Small molecule inhibitor-mediated targeting of rho-associated protein kinases may be a viable strategy to overcome cancer chemoresistance through down-regulation of survivin.
HIF1α regulates glioma chemosensitivity through the transformation between differentiation and dedifferentiation in various oxygen levels
TLDR
Hypoxia-inducible factor-1α (HIF1α) contributes substantially to the stemness maintenance of GSCs and resistance of glioma cells to chemotherapy in different oxygen levels, which highlights a novel viewpoint onglioma chemosensitivity from the transformation between dedifferentiation and differentiation inDifferent oxygen levels.
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Immunohistochemical analysis of 44 malignant glioma specimens showed significant positive correlation between expression levels of MGMT and phosphorylated STAT3, suggesting STAT3 inhibitor might be one of the candidate reagents for combination therapy with temozolomide for patients with Templo-resistant GBM.
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TLDR
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TLDR
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