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Glioblastoma multiforme (GBM) is the most common type of primary brain tumour in adults, and presents a very low survival rate. Isocitrate dehydrogenase (IDH)1/2 mutations have been found in ~12% of glioblastomas and are associated with long-term GBM survival. However, the risk factors that influence the prognosis of IDH-wild type GBM remain unclear. Hypoxia-inducible factor (HIF)-1α, an important oxygen-regulated transcription factor, has been demonstrated to serve a crucial role in tumour development and to be associated with a poor prognosis. In addition, caveolin-1 (CAV1) is a plasma membrane organizing protein, the expression of which can also be regulated by a hypoxic microenvironment. The present study therefore aimed to examine the expression levels of HIF-1α and CAV1, and their association with GBM prognosis. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to analyse the expression levels of HIF-1α and CAV1 in paired GBM tumour and adjacent non-tumour tissues. Immunohistochemistry was used to analyse the expression of the two proteins in paraffin-embedded tissues obtained from 42 patients with IDH-wild type GBM. Statistical analyses were performed to examine the correlation between HIF-1α and CAV1 expression and patient prognosis. The results revealed hat the expression levels of HIF-1α and CAV1 were upregulated in IDH-wild type GBM tissues compared to their paired non-tumour tissues (P<0.001). The expression of CAV1 was significantly correlated with high HIF-1α expression (P<0.01). In addition, overexpression of HIF-1α and CAV1 was markedly associated with a poor prognosis (P<0.001). In conclusion, HIF-1α and CAV1 may represent potential biomarkers for IDH-wild type GBM prognosis and potential targets for the development of therapies extending GBM survival. [ABSTRACT FROM AUTHOR]

Brain-type glycogen phosphorylase (PYGB) is an enzyme that metabolizes glycogen, whose function is to provide energy for an organism in an emergency state. The present study purposed to investigate the role and mechanism of PYGB silencing on the growth and apoptosis of prostate cancer cells. A cell counting kit-8 assay and flow cytometry were performed to determine the cell viability, apoptosis and reactive oxygen species (ROS) content, respectively. Colorimetry was performed to analyze the activity of caspase-3. Western blotting and reverse transcription-quantitative polymerase chain reaction were used to evaluate the associated mRNA and protein expression levels. The results revealed that PYGB was upregulated in prostate cancer tissues and was associated with disease progression. In addition, PYGB silencing suppressed the cell viability of PC3 cells. PYGB silencing promoted apoptosis of PC3 cells via the regulation of the expression levels of cleaved-poly (adenosine diphosphate-ribose) polymerase, cleaved-caspase-3, B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein. PYGB silencing increased the ROS content in PC3 cells, and affected nuclear factor (NF)-κB/nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathways in PC3 cells. In conclusion, PYGB silencing suppressed the growth and promoted the apoptosis of prostate cancer cells by affecting the NF-κB/Nrf2 signaling pathway. The present study provided evidence that may lead to the development of a potential therapeutic strategy for prostate cancer. [ABSTRACT FROM AUTHOR]