The importance of pragmatism in delivering teaching

Bajgoric, Sanjin

doi:10.1111/tct.12417

Cited by 1 publication

(1 citation statement)

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“…Induction of the JAK/STAT pathway may contribute to abnormal proliferative, invasive, and angiogenetic behaviors of glioblastoma cells, and SOCS family was indicated to be main inhibitors of JAK/STAT pathway (Martini et al, 2008). Another study has also found out that SOCS family can inhibit tumor progression via suppression of JAK/STAT pathway (Bajgoric, 2015). Among SOCS family members, SOCS3 has been observed to negatively regulate the JAK/STAT pathway and downregulation of SOCS3 is associated with an elevated level of STAT3 activation in epithelial ovarian cancer (Ying et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Silencing microRNA‐221/222 cluster suppresses glioblastoma angiogenesis by suppressor of cytokine signaling‐3‐dependent JAK/STAT pathway

Liu

Xiao

et al. 2019

Journal Cellular Physiology

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Angiogenesis is a major pathologic characteristic of glioblastoma, which is one aggressive primary brain tumor. cluster has been previously reported to function importantly in malignant glioma biological process. The current study aims at evaluating the effects of miR-221/222 cluster on angiogenesis of glioblastoma cells. Microarray data were analyzed to select glioblastoma-associated differentially expressed genes, and dual-luciferase reporter assay was performed to assess targeting correlation between miR-221/222 cluster and suppressor of cytokine signaling-3 (SOCS3). Subsequently, the expression patterns of miR-221 and miR-222 in glioblastoma cells were identified. miR-221 and miR-222 were overexpressed or silenced in glioblastoma cells to identify the effect of miR-221/222 cluster in cell invasion, migration, proliferation, and angiogenesis. To define downstream pathway of miR-221/222 cluster or SOCS3 in glioblastoma, levels of Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway-related proteins were assessed. Additionally, the functions of miR-221/222 on glioblastoma cell angiogenesis were measured in vivo with microvessel density assayed. miR-221 and miR-222 were expressed at a high level and SOCS3 was at a low level in glioblastoma. Downregulation of the miR-221/222 cluster diminished the invasion, migration, proliferation, and angiogenesis with reduced protein levels of matrix metalloproteinase-2 (MMP-2), MMP-9, and vascular endothelial growth factor in glioblastoma cells. Also, silencing miR-221/ 222 cluster reduced p-JAK2/JAK2 and p-STAT3/STAT3. Consistently, the inhibitory role of silencing miR-221/222 cluster on tumorigenesis of glioblastoma cells was confirmed in vivo. Collectively, the inhibition of miR-221/222 cluster could attenuate the glioblastoma angiogenesis through inactivation of the JAK/STAT pathway by upregulating SOCS3. K E Y W O R D S angiogenesis, glioblastoma, janus kinase/signal transducers and activators of transcription pathway, microRNA-221/222 cluster, suppressor of cytokine signaling-3

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Section: Discussionmentioning

confidence: 99%