Effect of serum depletion on centrosome overduplication and death of human pancreatic cancer cells after exposure to radiation

Shono, Masaki; Sato, Norihiro; Mizumoto, Kazuhiro; Minamishima, Yoji Andrew; Nakamura, Masafumi; Maehara, Naoki; Urashima, Taro; Saimura, Michiyo; Qian, Liwu; Nishio, Shoko; Nagai, Eishi; Tanaka, Masao

doi:10.1016/s0304-3835(01)00533-x

Cited by 5 publications

(4 citation statements)

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“…Although in vitro cell culture experiments and treatments are done in absence of serum, few studies have focused on the influence of serum depletion on cellular response [3], but recent results do suggest that it is not simply mediated by growth arrest but controlled by unknown regulatory proteins [46]. A synergistic effect between serum and insulin or insulin-like growth factor-I (IGF-I) is seen in choriocarcinoma cells [47].…”

Section: Discussionmentioning

confidence: 99%

“…Serum depletion can influence the radiation-induced killing of pancreatic cancer cells [3], allow the dexamethasone-mediated differentiation of neuroblastoma cells [4], and give rise to growth inhibition, differentiation and interleukin 1 receptor expression in leukemia cells [5]. However, the effect of serum depletion on trophoblast function remains unknown.…”

Section: Introductionmentioning

confidence: 99%

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Serum depletion induces changes in protein expression in the trophoblast-derived cell line HTR-8/SVneo

et al. 2016

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BackgroundHow nutrition and growth factor restriction due to serum depletion affect trophoblast function remains poorly understood. We performed a proteomic differential study of the effects of serum depletion on a first trimester human immortalized trophoblast cell line.MethodsThe viability of HTR-8/SVneo trophoblast cells in culture with 0, 0.5 and 10 % fetal bovine serum (FBS) were assayed via MTT at 24, 48 and 64 h. A comparative proteomic analysis of the cells grown with those FBS levels for 24 h was performed using two-dimensional electrophoresis (2DE), followed by mass spectrometry for protein spot identification, and a database search and bioinformatics analysis of the expressed proteins. Differential spots were identified using the Kolmogorov-Smirnov test (n = 3, significance level 0.10, D > 0.642) and/or ANOVA (n = 3, p < 0.05).ResultsThe results showed that low serum doses or serum depletion differentially affect cell growth and protein expression. Differential expression was seen in 25 % of the protein spots grown with 0.5 % FBS and in 84 % of those grown with 0 % FBS, using 10 % serum as the physiological control. In 0.5 % FBS, this difference was related with biological processes typically affected by the serum, such as cell cycle, regulation of apoptosis and proliferation. In addition to these changes, in the serum-depleted proteome we observed downregulation of keratin 8, and upregulation of vimentin, the glycolytic enzymes enolase and pyruvate kinase (PKM2) and tumor progression-related inosine-5’-monophosphate dehydrogenase 2 (IMPDH2) enzyme. The proteins regulated by total serum depletion, but not affected by growth in 0.5 % serum, are members of the glycolytic and nucleotide metabolic pathways and the epithelial-to-mesenchymal transition (EMT), suggesting an adaptive switch characteristic of malignant cells.ConclusionsThis comparative proteomic analysis and the identified proteins are the first evidence of a protein expression response to serum depletion in a trophoblast cell model. Our results show that serum depletion induces specific changes in protein expression concordant with main cell metabolic adaptations and EMT, resembling the progression to a malignant phenotype.Electronic supplementary materialThe online version of this article (doi:10.1186/s11658-016-0018-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Serum depletion induces changes in protein expression in the trophoblast-derived cell line HTR-8/SVneo

et al. 2016

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“…The irradiation causes centrosomal overduplication and multipolar spindles. Irradiated pancreatic cancer cells treated with serum depletion exhibited an increase in the number of centrosomal abnormalities, which promoted nuclear fragmentation and cell death (32).…”

Section: Diagnosis and Treatmentmentioning

confidence: 99%

Centrosomal Abnormalities in Pancreatic Cancer: Molecular Mechanisms and Clinical Implications

Ansari

Bellido

Bauden

et al. 2018

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“…Compromised TGF-b production or signaling in either murine keratinocytes or human mammary epithelial cells induces elevated centrosomal amplification in spite of functional p53 within these non-malignant epithelial cells (authors' unpublished observations). Centrosomal amplification subsequent to irradiation has been reported in cancer cell lines of various species and is almost invariably associated with a prolonged G2 cell cycle arrest (Sato et al 1983, Shono et al 2001, Dodson et al 2004, Kawamura et al 2004, Yoon et al 2005. Interestingly, the absence of exogenous TGF-b sensitizes irradiated, p53-competent human mammary epithelial cells (HMEC) to persistent centrosomal amplification and the addition of TGF-b impairs the permanence, but not induction, of these abnormalities (authors' unpublished observations).…”

Section: Tgf-b and Its Dual Role In Cancermentioning

confidence: 99%

The pleiotropic roles of transforming growth factor beta in homeostasis and carcinogenesis of endocrine organs

Fleisch¹,

Maxwell²,

Barcellos-Hoff³

2006

Endocr Relat Cancer

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Transforming growth factor b (TGF-b) is a ubiquitous cytokine that plays a critical role in numerous pathways regulating cellular and tissue homeostasis. TGF-b is regulated by hormones and is a primary mediator of hormone response in uterus, prostate and mammary glands. This review will address the role of TGF-b in regulating hormone-dependent proliferation and morphogenesis. The subversion of TGF-b regulation during the processes of carcinogenesis, with particular emphasis on its effects on genetic stability and epithelial to mesenchymal transition, will also be examined. An understanding of the multiple and complex mechanisms of TGF-b regulation of epithelial function, and the ultimate loss of TGF-b function during carcinogenesis, will be critical in the design of novel therapeutic interventions for endocrine-related cancers.

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Effect of serum depletion on centrosome overduplication and death of human pancreatic cancer cells after exposure to radiation

Cited by 5 publications

References 28 publications

Serum depletion induces changes in protein expression in the trophoblast-derived cell line HTR-8/SVneo

Serum depletion induces changes in protein expression in the trophoblast-derived cell line HTR-8/SVneo

Centrosomal Abnormalities in Pancreatic Cancer: Molecular Mechanisms and Clinical Implications

The pleiotropic roles of transforming growth factor beta in homeostasis and carcinogenesis of endocrine organs

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