AI Article Synopsis
- PPM1B acts as a phosphatase for IKKβ, playing a critical role in regulating NF-κB signaling, which is often activated in glioma cells.
- The study discovered that lower levels of PPM1B in glioma tissues correlate with worse patient survival, suggesting its importance in cancer prognosis.
- Overexpressing PPM1B can inhibit glioma cell growth, induce cell death, and improve response to the chemotherapy drug temozolomide, both in cell cultures and in animal models.
Article Abstract
Protein phosphatase magnesium-dependent 1B (PPM1B) functions as IKKβ phosphatases to terminate nuclear factor kappa B (NF-κB) signaling. NF-κB signaling was constitutively activated in glioma cells. At present, little is known about the role of PPM1B in glioma. In the current study, we found that the expression of PPM1B was reduced in glioma tissues and cells, and decreased expression of PPM1B was related to poor overall survival of patients. Overexpression of PPM1B inhibited the proliferation and promoted apoptosis of glioma cells. Moreover, PPM1B overexpression reduced the phosphorylation of IKKβ and inhibited the nuclear localization of NF-κBp65. PDTC, an inhibitor of NF-κB signaling, reversed PPM1B-knockdown-induced cell proliferation. Furthermore, overexpression of PPM1B enhanced the sensitivity of glioma cells to temozolomide. In vivo experiments showed that overexpression of PPM1B could inhibit tumor growth, improve the survival rate of nude mice, and enhance the sensitivity to temozolomide. In conclusion, PPM1B suppressed glioma cell proliferation and the IKKβ-NF-κB signaling pathway, and enhanced temozolomide sensitivity of glioma cells.
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| http://dx.doi.org/10.1002/cbin.12092 | DOI Listing |
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