GLTSCR2 contributes to the death resistance and invasiveness of hypoxia-selected cancer cells |
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Authors: | Jee-Youn KimJae-Hoon Park Sun Lee |
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Affiliation: | Department of Pathology, School of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea |
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Abstract: | Tumor hypoxia may be an indicator of poor survival in cancer patients. Thus, an understanding of the molecular mechanism responsible for hypoxic tumor selection is essential to gain further insight into tumor biology. Our aim in this study was to investigate whether hypoxia-responsive GLTSCR2 contributes to death resistance and increased invasiveness of hypoxia-selected glioblastoma cells. We found that repeated hypoxia downregulates p53-upstream regulator, GLTSCR2, which resulted in increased death resistance and invasive potential of glioblastoma cells. Restoration of GLTSCR2 expression suppressed the malignant potential of hypoxia-selected cells. Our results indicate that GLTSCR2 participates in hypoxia-induced malignant potential. |
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Keywords: | ARF, alternative reading frame GLTSCR2, glioblastoma tumor suppressive candidate region gene 2 JNK, c-jun N-terminal kinase MDM2, murine double minute 2 NPM, nucleophosmin Pict-1, Protein interacting with C-terminus-1 PTEN, phosphatase and tensin homolog RPL11, ribosomal protein L11 |
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