p38γ overexpression in gliomas and its role in proliferation and apoptosis

Yang, Kui; Liu, Yunsheng; Liu, Zhixiong; Liu, Jinfang; Liu, Xin; Chen, Xin; Li, Chuntao; Zeng, Yu

doi:10.1038/srep02089

Cited by 28 publications

(17 citation statements)

References 32 publications

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“…A study by Shervington et al[ 9 ] in glioma patients, showed a significant difference in telomerase protein levels between cancerous and normal tissues. Also, in line with our finding, IHC based hTERT expression pattern has been reported on low and high grade glioma samples, indicating higher expression to be linked with grade progression[ 10 ]. The analysis of our marker indicates that measurement of precise proliferative activity is crucial to delineate the transition from low to high grade OA.…”

Section: Discussionsupporting

confidence: 90%

Unique case of oligoastrocytoma with recurrence and grade progression: Exhibiting differential expression of high mobility group-A1 and human telomerase reverse transcriptase

Gandhi¹,

Khare²,

Niraj³

et al. 2016

WJCC

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Mixed gliomas, primarily oligoastrocytomas, account for about 5%-10% of all gliomas. Distinguishing oligoastrocytoma based on histological features alone has limitations in predicting the exact biological behavior, necessitating ancillary markers for greater specificity. In this case report, human telomerase reverse transcriptase (hTERT) and high mobility group-A1 (HMGA1); markers of proliferation and stemness, have been quantitatively analyzed in formalin-fixed paraffin-embedded tissue samples of a 34 years old patient with oligoastrocytoma. Customized florescence-based immunohistochemistry protocol with enhanced sensitivity and specificity is used in the study. The patient presented with a history of generalized seizures and his magnetic resonance imaging scans revealed infiltrative ill-defined mass lesion with calcified foci within the left frontal white matter, suggestive of glioma. He was surgically treated at our center for four consecutive clinical events. Histopathologically, the tumor was identified as oligoastrocytoma-grade II followed by two recurrence events and final progression to grade III. Overall survival of the patient without adjuvant therapy was more than 9 years. Glial fibrillary acidic protein, p53, Ki-67, nuclear atypia index, pre-operative neutrophil-lymphocyte ratio, are the other parameters assessed. Findings suggest that hTERT and HMGA1 are linked to tumor recurrence and progression. Established markers can assist in defining precise histopathological grade in conjuction with conventional markers in clinical setup.

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Section: Discussionsupporting

confidence: 90%

Unique case of oligoastrocytoma with recurrence and grade progression: Exhibiting differential expression of high mobility group-A1 and human telomerase reverse transcriptase

Gandhi¹,

Khare²,

Niraj³

et al. 2016

WJCC

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“…Expression of siRNA or shRNA targeting p38 transcripts offers a feasible solution for reducing p38 levels when neither kinase inhibitors nor genetic alteration on the DNA levels is possible or desired. RNA interference has been used for all p38 transcripts in the past ( Sumara et al, 2009 ; Yang et al, 2013 ; Stefanoska et al, 2018 ) and offers gene-specific reduction in p38 transcript and protein levels. Cell type-specific or brain region-specific isoform-selective RNA interference likely will see increased use to explore functions of p38-regulated pathways in vivo in future studies.…”

Section: Central Methods To Study P38 Kinasesmentioning

confidence: 99%

Functions of p38 MAP Kinases in the Central Nervous System

Asih

Prikas

Stefanoska

et al. 2020

Front. Mol. Neurosci.

111

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Mitogen-activated protein (MAP) kinases are a central component in signaling networks in a multitude of mammalian cell types. This review covers recent advances on specific functions of p38 MAP kinases in cells of the central nervous system. Unique and specific functions of the four mammalian p38 kinases are found in all major cell types in the brain. Mechanisms of p38 activation and downstream phosphorylation substrates in these different contexts are outlined and how they contribute to functions of p38 in physiological and under disease conditions. Results in different model organisms demonstrated that p38 kinases are involved in cognitive functions, including functions related to anxiety, addiction behavior, neurotoxicity, neurodegeneration, and decision making. Finally, the role of p38 kinases in psychiatric and neurological conditions and the current progress on therapeutic inhibitors targeting p38 kinases are covered and implicate p38 kinases in a multitude of CNS-related physiological and disease states.

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“…Recently, p38γ MAPK has emerged as an oncogenic MAPK (MAPK) [2–6]. It was also found to be highly expressed in some human cancer cells [4, 5, 7, 8]. p38γ MAPK is shown to be involved in the regulation of cancer stem cells (CSCs), migration/invasion, tumorigenesis, and cell transformation [2–6, 9, 10].…”

Section: Introductionmentioning

confidence: 99%

Role of p38γ MAPK in regulation of EMT and cancer stem cells

Wang

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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p38γ is a member of p38 MAPK family which contains four isoforms p38α, p38β, p38γ, and p38δ. p38γ MAPK has unique function and is less investigated. Recent studies revealed that p38γ MAPK may be involved in tumorigenesis and cancer aggressiveness. However, the underlying cellular/molecular mechanisms remain unclear. Epithelial-mesenchymal transition (EMT) is a process that epithelial cancer cells transform to facilitate the loss of epithelial features and gain of mesenchymal phenotype. EMT promotes cancer cell progression and metastasis, and is involved in the regulation of cancer stem cells (CSCs) which have self-renewal capacity and are resistant to chemotherapy and target therapy. We showed that p38γ MAPK significantly increased EMT in breast cancer cells; over-expression of p38γ MAPK enhanced EMT while its down-regulation inhibited EMT. Meanwhile, p38γ MAPK augmented CSC population while knock down of p38γ MAPK decreased CSC ratio in breast cancer cells. MicroRNA-200b (miR-200b) was down-stream of p38γ MAPK and inhibited by p38γ MAPK; miR-200b mimics blocked p38γ MAPK-induced EMT while miR-200b inhibitors promoted EMT. p38γ MAPK regulated miR-200b through inhibiting GATA3. p38γ MAPK induced GATA3 ubiquitination, leading to its proteasome-dependent degradation. Suz12, a Polycomb group protein, was down-stream of miR-200b and involved in miR-200b regulation of EMT. Thus, our study established an important role of p38γ MAPK in EMT and identified a novel signaling pathway for p38γ MAPK-mediated tumor promotion.

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p38γ overexpression in gliomas and its role in proliferation and apoptosis

Cited by 28 publications

References 32 publications

Unique case of oligoastrocytoma with recurrence and grade progression: Exhibiting differential expression of high mobility group-A1 and human telomerase reverse transcriptase

Unique case of oligoastrocytoma with recurrence and grade progression: Exhibiting differential expression of high mobility group-A1 and human telomerase reverse transcriptase

Functions of p38 MAP Kinases in the Central Nervous System

Role of p38γ MAPK in regulation of EMT and cancer stem cells

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