Tethering Function of the Caspase Cleavage Fragment of Golgi Protein p115 Promotes Apoptosis via a p53-dependent Pathway

How, Poh Choo; Shields, Dennis

doi:10.1074/jbc.m110.175174

Cited by 22 publications

(22 citation statements)

References 55 publications

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“…Nowadays, mechanism studies on the tumor apoptosis inhibition have drawn more and more attention. The studies on USO1 in mitosis and apoptosis revealed that USO1 was cleaved by caspase3 pathway and promoted cell apoptosis which is related to p53 signaling pathway [19,20]. Our results are consistent with the previous reports, but whether there are other proteins interacting with USO1 involved in cell proliferation and apoptosis in colon cancer still needs further research.…”

Section: Discussionsupporting

confidence: 94%

Lentivirus-mediated silencing of USO1 inhibits cell proliferation and migration of human colon cancer cells

Sui

Xing

et al. 2015

Med Oncol

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Belonging to the tether factors family, USO1 (vesicle transport factor) plays a critical role in endoplasmic reticulum-Golgi trafficking and vesicular transport which is important to tumorigenesis. However, the mechanism of USO1 in colon cancer was still unknown. In our research, the expression of USO1 was knockdown in colon cancer cells (HCT116 and HT-29) by using a special lentivirus shRNA approach. A series of experiments were carried out to evaluate the effect of deregulation of USO1, including cell proliferation, apoptosis, cell migration and cell cycle. Knockdown of USO1 inhibits the ability of cell proliferation and migration. Furthermore, the deregulation of USO1 induces early apoptosis and decreased cells in G2-M phase. We demonstrate for the first time that USO1 gene has a critical role in human colon cancer. Our finding represents that USO1 gene may be a promising target for therapy and diagnosis in treatment of human colon cancer.

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Section: Discussionsupporting

confidence: 94%

Lentivirus-mediated silencing of USO1 inhibits cell proliferation and migration of human colon cancer cells

Sui

Xing

et al. 2015

Med Oncol

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“…It was shown that expression of the CTF leads to the phosphorylation and stabilization of p53 and results in the expression of Puma. CTF expression also promotes p53-ERK interaction, which amplifies the apoptotic signal [152]. …”

Section: P53 and Apoptosismentioning

confidence: 99%

p53 and Ceramide as Collaborators in the Stress Response

Hage‐Sleiman

Esmerian

Kobeissy

et al. 2013

IJMS

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The sphingolipid ceramide mediates various cellular processes in response to several extracellular stimuli. Some genotoxic stresses are able to induce p53-dependent ceramide accumulation leading to cell death. However, in other cases, in the absence of the tumor suppressor protein p53, apoptosis proceeds partly due to the activity of this “tumor suppressor lipid”, ceramide. In the current review, we describe ceramide and its roles in signaling pathways such as cell cycle arrest, hypoxia, hyperoxia, cell death, and cancer. In a specific manner, we are elaborating on the role of ceramide in mitochondrial apoptotic cell death signaling. Furthermore, after highlighting the role and mechanism of action of p53 in apoptosis, we review the association of ceramide and p53 with respect to apoptosis. Strikingly, the hypothesis for a direct interaction between ceramide and p53 is less favored. Recent data suggest that ceramide can act either upstream or downstream of p53 protein through posttranscriptional regulation or through many potential mediators, respectively.

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“…Caspase‐9 plays a major role in p53‐dependent apoptosis (Hakem et al, 1998; Kuida et al, 1998; How and Shields, 2011). We therefore investigated whether the caspase‐9 pathway was targeted by p53 in DNA‐damaging drug‐induced apoptosis sensitized by N‐myc in SHEP1 cells.…”

Section: Resultsmentioning

confidence: 99%

DNA‐damaging drug‐induced apoptosis sensitized by N‐myc in neuroblastoma cells

Wang

Gong

et al. 2012

Cell Biology International

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Neuroblastoma is one of the most common solid tumours in children (8-10% of all malignancies). Over 22% of cases have N-myc amplification associated with aggressively growing neuroblastomas. Oncogene-induced sensitization of cells to apoptosis is an important mechanism for suppression of tumorigenesis. Tumour suppressors often play a critical role in linking oncogenes to apoptotic machinery. For example, activated p53 then targets both intrinsic and extrinsic pathways to promote apoptosis through transcription-dependent and -independent mechanisms. Understanding of the involved mechanisms has important clinical implications. We have employed DNA-damaging drug-induced apoptosis sensitized by oncogene N-myc as a model. DNA damaging drugs trigger high levels of p53, leading to caspase-9 activation in neuroblastoma cells. Inactivation of p53 protects cells from drug-triggered apoptosis sensitized by N-myc. These findings thus define a molecular pathway for mediating DNA-damaging drug-induced apoptosis sensitized by oncogene, and suggest that inactivation of p53 or other components of this apoptotic pathway may confer drug resistance in neuroblastoma cells. The data also suggests that inactivation of apoptotic pathways through co-operating oncogenes may be necessary for the pathogenesis of neuroblastoma with N-myc amplification.

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Tethering Function of the Caspase Cleavage Fragment of Golgi Protein p115 Promotes Apoptosis via a p53-dependent Pathway

Cited by 22 publications

References 55 publications

Lentivirus-mediated silencing of USO1 inhibits cell proliferation and migration of human colon cancer cells

Lentivirus-mediated silencing of USO1 inhibits cell proliferation and migration of human colon cancer cells

p53 and Ceramide as Collaborators in the Stress Response

DNA‐damaging drug‐induced apoptosis sensitized by N‐myc in neuroblastoma cells

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