Glioma: What is the role of c-Myc, hsp90 and telomerase?

Shervington, Amal; Cruickshanks, Nichola; Wright, Hamish; Atkinson-Dell, Rebecca; Lea, Robert; Roberts, Gareth; Shervington, Leroy Alexander

doi:10.1007/s11010-006-2495-z

Cited by 38 publications

(31 citation statements)

References 60 publications

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“…c-Myc is a transcription factor important in the regulation of both cell proliferation and cell death [66]. Even though c-Myc progresses the cell cycle from G1 phase to S phase, it also induces apoptosis when expressed under growth inhibitory conditions, such as lack of growth factors [67].…”

Section: Discussionmentioning

confidence: 99%

Large Scale Hippocampal Cellular Distress may Explain the Behavioral Consequences of Repetitive Traumatic Experiences-A Proteomic Approach

et al. 2008

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Early life traumatic experiences are associated with psychopathology in adulthood. This may be due in part to the effects of trauma on hippocampal development and protein expression. The purpose of the study was to investigate the effects of early life trauma and adult re-stress on ventral hippocampal protein expression. Adolescent rats (n = 19) were subjected to a triple stressor on post-natal day 28 followed 7 days later by the first re-stress session and 25 days later (post-natal day 60 = adulthood) by the second re-stress session. Ventral hippocampi were collected on post-natal day 68 for protein expression determinations using protein arrays and 2D-gel electrophoresis with liquid chromatography tandem mass spectrometry. Compared to controls, traumatized animals showed an increase in Ca(2+) homeostatic proteins, dysregulated signaling pathways and energy metabolism enzymes, cytoskeletal protein changes, a decrease in neuroplasticity regulators, energy metabolism enzymes and an increase in apoptotic initiator proteins. These results indicate the extensive impact of trauma on adult brain development and behavior.

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Section: Discussionmentioning

confidence: 99%

Large Scale Hippocampal Cellular Distress may Explain the Behavioral Consequences of Repetitive Traumatic Experiences-A Proteomic Approach

et al. 2008

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“…This is consistent with Klu recognizing a distinct consensus DNA binding sequence to WT1. However, we cannot rule out the possibility that the inability of the WT1 transgenic protein to induce supernumerary type II neuroblasts is simply due to the absence of necessary co-factors in the fly, as repression of target gene transcription by WT1 requires additional co-factors in vertebrates (Shervington et al, 2006). More studies will be necessary to elucidate the molecular function of Klu in promoting type II neuroblast identity.…”

Section: Regulation Of Inp Maturationmentioning

confidence: 97%

klumpfuss distinguishes stem cells from progenitor cells during asymmetric neuroblast division

2012

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SUMMARYAsymmetric stem cell division balances maintenance of the stem cell pool and generation of diverse cell types by simultaneously allowing one daughter progeny to maintain a stem cell fate and its sibling to acquire a progenitor cell identity. A progenitor cell possesses restricted developmental potential, and defects in the regulation of progenitor cell potential can directly impinge on the maintenance of homeostasis and contribute to tumor initiation. Despite their importance, the molecular mechanisms underlying the precise regulation of restricted developmental potential in progenitor cells remain largely unknown. We used the type II neural stem cell (neuroblast) lineage in Drosophila larval brain as a genetic model system to investigate how an intermediate neural progenitor (INP) cell acquires restricted developmental potential. We identify the transcription factor Klumpfuss (Klu) as distinguishing a type II neuroblast from an INP in larval brains. klu functions to maintain the identity of type II neuroblasts, and klu mutant larval brains show progressive loss of type II neuroblasts due to premature differentiation. Consistently, Klu protein is detected in type II neuroblasts but is undetectable in immature INPs. Misexpression of klu triggers immature INPs to revert to type II neuroblasts. In larval brains lacking brain tumor function or exhibiting constitutively activated Notch signaling, removal of klu function prevents the reversion of immature INPs. These results led us to propose that multiple mechanisms converge to exert precise control of klu and distinguish a progenitor cell from its sibling stem cell during asymmetric neuroblast division.

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“…A variety of cell survival signaling mechanisms such as overexpression of inhibitor-of-apoptosis proteins (IAPs), nuclear factor kappa B (NFjD), and anti-apoptotic Bcl-2 proteins may play crucial roles to prevent apoptosis. On the contrary, inhibition of these factors favors apoptosis [9][10][11][12] and seems to be a good strategy for treating cancers including glioblastoma. New therapeutic strategies, which can synergistically inhibit the anti-apoptotic factors in tumor cells to facilitate apoptosis are warranted for the cure and management of this devastating disease.…”

Section: Introductionmentioning

confidence: 99%

Curcumin Suppressed Anti-apoptotic Signals and Activated Cysteine Proteases for Apoptosis in Human Malignant Glioblastoma U87MG Cells

2007

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Glioblastoma is the most malignant human brain tumor that shows poor response to existing therapeutic agents. Search continues for an effective therapy for controlling this deadliest brain tumor. Curcumin (CCM), a polyphenolic compound from Curcuma longa, possesses anti-cancer properties in both in vitro and in vivo. In the present investigation, we evaluated the therapeutic efficacy of CCM against human malignant glioblastoma U87MG cells. Trypan blue dye exclusion test showed decreased viability of U87MG cells with increasing dose of CCM. Wright staining and ApopTag assay, respectively, showed the morphological and biochemical features of apoptosis in U87MG cells treated with 25 microM and 50 microM of CCM for 24 h. Western blotting showed activation of caspase-8, cleavage of Bid to tBid, increase in Bax:Bcl-2 ratio, and release of cytochrome c from mitochondria followed by activation of caspase-9 and caspase-3 for apoptosis. Also, CCM treatments increased cytosolic level of Smac/Diablo to suppress the inhibitor-of-apoptosis proteins and down regulated anti-apoptotic nuclear factor kappa B (NFkappaB), favoring the apoptosis. Increased activities of calpain and caspase-3 cleaved 270 kDa alpha-spectrin at specific sites generating 145 kDa spectrin break down product (SBDP) and 120 kDa SBDP, respectively, leading to apoptosis in U87MG cells. Results show that CCM is an effective therapeutic agent for suppression of anti-apoptotic factors and activation of calpain and caspase proteolytic cascades for apoptosis in human malignant glioblastoma cells.

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Glioma: What is the role of c-Myc, hsp90 and telomerase?

Cited by 38 publications

References 60 publications

Large Scale Hippocampal Cellular Distress may Explain the Behavioral Consequences of Repetitive Traumatic Experiences-A Proteomic Approach

Large Scale Hippocampal Cellular Distress may Explain the Behavioral Consequences of Repetitive Traumatic Experiences-A Proteomic Approach

klumpfuss distinguishes stem cells from progenitor cells during asymmetric neuroblast division

Curcumin Suppressed Anti-apoptotic Signals and Activated Cysteine Proteases for Apoptosis in Human Malignant Glioblastoma U87MG Cells

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