Overexpression of apoptosis‐associated speck‐like protein in P388D1 murine lymphoma cells affects metastatic properties

Zhang, Yi; Zhang, Jian; Lin, Changwei; Wei, Wei; Ren, Shuo; Zuo, Yongchun

doi:10.1002/hon.1010

Cited by 4 publications

(3 citation statements)

References 24 publications

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“…On the other hand, the results of this study also suggested the possible relationship between ASC expression and metastasis, although the relationship between ASC score and Nclassification was not statistically significant (univariate analysis, P ¼ .053). Zhang et al 32 reported that overexpression of ASC resulted in reduced cancer metastasis to the lung and liver of mice. Termén et al 33 reported that p53 regulated epithelial-mesenchymal transition (EMT) induced by transforming growth factor b.…”

Section: Oral and Maxillofacial Pathology Oooomentioning

confidence: 98%

Clinical significance of apoptosis-associated speck-like protein containing a caspase recruitment domain in oral squamous cell carcinoma

Shimane

Kobayashi

Takeoka³

et al. 2013

Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology

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Section: Oral and Maxillofacial Pathology Oooomentioning

confidence: 98%

Clinical significance of apoptosis-associated speck-like protein containing a caspase recruitment domain in oral squamous cell carcinoma

Shimane

Kobayashi

Takeoka³

et al. 2013

Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology

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“…Colorectal cancer was enhanced upon genetic deletion of caspase-1 or ASC [14], while ASC-overexpressing lymphoma cells showed reduced metastasis [15]. The understanding of the mechanisms of ASC has progressed as well, with reports of tumorigenesis inhibition in primary melanoma via ASC expression by restricting NF-κB activity [16] and decreased P53- and p21-related cell apoptosis by knockdown of ASC [17].…”

Section: Introductionmentioning

confidence: 99%

ASC Induces Apoptosis via Activation of Caspase-9 by Enhancing Gap Junction-Mediated Intercellular Communication

Kitazawa¹,

Hida²,

Fujii³

et al. 2017

PLoS ONE

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ASC (apoptosis-associated speck-like protein containing a CARD) is a key adaptor molecule of inflammasomes that mediates inflammatory and apoptotic signals. Aberrant methylation-induced silencing of ASC has been observed in a variety of cancer cells, thus implicating ASC in tumor suppression, although this role remains incompletely defined especially in the context of closely neighboring cell proliferation. As ASC has been confirmed to be silenced by abnormal methylation in HT1080 fibrosarcoma cells as well, this cell line was investigated to characterize the precise role and mechanism of ASC in tumor progression. The effects of ASC were examined using in vitro cell cultures based on comparisons between low and high cell density conditions as well as in a xenograft murine model. ASC overexpression was established by insertion of the ASC gene into pcDNA3 and pMX-IRES-GFP vectors, the latter being packed into a retrovirus and subjected to reproducible competitive assays using parental cells as an internal control, for evaluation of cell viability. p21 and p53 were silenced using shRNA. Cell viability was suppressed in ASC-expressing transfectants as compared with control cells at high cell density conditions in in vitro culture and colony formation assays and in in vivo ectopic tumor formation trials. This suppression was not detected in low cell density conditions. Furthermore, remarkable progression of apoptosis was observed in ASC-introduced cells at a high cell density, but not at a low one. ASC-dependent apoptosis was mediated not by p21, p53, or caspase-1, but rather by cleavage of caspase-9 as well as by suppression of the NF-κB-related X-linked inhibitor-of-apoptosis protein. Caspase-9 cleavage was observed to be dependent on gap junction formation. The remarkable effect of ASC on the induction of apoptosis through caspase-9 and gap junctions revealed in this study may lead to promising new approaches in anticancer therapy.

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“…Greater than 80% of the tumors found were adenoma with ~10% of the tumor found to be lymphomas in the 0.04 Gy and ~10% of the tumor in the 0.08 Gy group classified as histiocytic sarcomas. The lymphomas from these animals were likely due to metastases from other tumor sites such as spleen or thymus in the same animals [ 35 ].…”

Section: Resultsmentioning

confidence: 99%

Heavy-Ion-Induced Lung Tumors: Dose- & LET-Dependence

Chang

Bakke

Rosen

et al. 2022

Life

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There is a limited published literature reporting dose-dependent data for in vivo tumorigenesis prevalence in different organs of various rodent models after exposure to low, single doses of charged particle beams. The goal of this study is to reduce uncertainties in estimating particle-radiation-induced risk of lung tumorigenesis for manned travel into deep space by improving our understanding of the high-LET-dependent dose-response from exposure to individual ion beams after low particle doses (0.03–0.80 Gy). Female CB6F1 mice were irradiated with low single doses of either oxygen, silicon, titanium, or iron ions at various energies to cover a range of dose-averaged LET values from 0.2–193 keV/µm, using 137Cs γ-rays as the reference radiation. Sham-treated controls were included in each individual experiment totally 398 animals across the 5 studies reported. Based on power calculations, between 40–156 mice were included in each of the treatment groups. Tumor prevalence at 16 months after radiation exposure was determined and compared to the age-matched, sham-treated animals. Results indicate that lung tumor prevalence is non-linear as a function of dose with suggestions of threshold doses depending on the LET of the beams. Histopathological evaluations of the tumors showed that the majority of tumors were benign bronchioloalveolar adenomas with occasional carcinomas or lymphosarcomas which may have resulted from metastases from other sites.

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Overexpression of apoptosis‐associated speck‐like protein in P388D1 murine lymphoma cells affects metastatic properties

Cited by 4 publications

References 24 publications

Clinical significance of apoptosis-associated speck-like protein containing a caspase recruitment domain in oral squamous cell carcinoma

Clinical significance of apoptosis-associated speck-like protein containing a caspase recruitment domain in oral squamous cell carcinoma

ASC Induces Apoptosis via Activation of Caspase-9 by Enhancing Gap Junction-Mediated Intercellular Communication

Heavy-Ion-Induced Lung Tumors: Dose- & LET-Dependence

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