Molecular mechanism underlying differential apoptosis between human melanoma cell lines UACC903 and UACC903(+6) revealed by mitochondria-focused cDNA microarrays

Zhang, Qiuyang; Jun, Wu; Nguyen, AnhThu; Wang, Bi-Dar; He, Ping; Laurent, Georges St.; Rennert, Owen M.; Su, Yan

doi:10.1007/s10495-008-0231-8

Cited by 15 publications

(17 citation statements)

References 40 publications

(43 reference statements)

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“…cslab.ece.ntua.gr), the online resources for in-silico miRNA target prediction and pathway analysis, we looked up whether miR-125b targets messenger RNAs relevant for MM. Among hundreds of theoretical targets for miR125b, we found ErbB, Notch, p53, and mitogen-activated protein kinase-signaling pathways, including AKT3, MCL1, BCL2, PPP2CA, Notch 2, and members of the ErbB family (Table 3) [20][21][22][23][24][25][26].…”

Section: Resultsmentioning

confidence: 99%

Downregulation of miR-125b in metastatic cutaneous malignant melanoma

Glud¹,

Rossing²,

Hother³

et al. 2010

Melanoma Research

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This study aimed to identify microRNA species involved in the earliest metastatic event in cutaneous malignant melanoma (MM). Samples from 28 patients with MM [stage T2 (tumor), M0 (distant metastasis)] were grouped by the presence of micrometastasis in the sentinel lymph nodes (N0/N1). Melanoma cells were harvested from primary, cutaneous MM tumors by laser-capture microdissection, and microRNA expression profiles were obtained by the microarray technique. Results were validated by quantitative reverse transcription PCR. We found that miR-125b was downregulated in the primary cutaneous melanomas that produced early metastases (T2, N1, M0) compared with the sentinel lymph node-negative (T2, N0, M0) melanomas. MiR-125b has earlier been found to be downregulated in other tumor types and in atypic naevi compared with the common acquired naevi. In conclusion, miR-125b may be involved in an early progression of cutaneous MM.

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Section: Resultsmentioning

confidence: 99%

Downregulation of miR-125b in metastatic cutaneous malignant melanoma

Glud¹,

Rossing²,

Hother³

et al. 2010

Melanoma Research

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“…Because use of 3 replicates in cDNA microarrays analysis of even a single specimen greatly reduces misclassification rates 29, the hMitChip3 genes were all measured 9 times (3 identical probes per microarray and 3 microarray experiments per specimen), which generated reliable expression data for further analysis. The microarray data of 4,080 spots across all 36 gene chips used for 12 RNA samples were filtered by uniform statistic and bioinformatic criteria as described previously 24;30, which generated 800 genes with informative expression profiles. The supplemental table 1 reports the expression data of the selected 800 genes in each of the triplicate experiments before and after normalization as the raw and processed data, respectively; while Figure 1 shows the box plots of mRNA levels of 800 genes before and after the data normalization.…”

Section: Resultsmentioning

confidence: 99%

Dysregulated Mitochondrial Genes and Networks with Drug Targets in Postmortem Brain of Patients with Posttraumatic Stress Disorder (PTSD) Revealed by Human Mitochondria-Focused cDNA Microarrays

Jun²,

Zhang³

et al. 2008

Int. J. Biol. Sci.

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103

110

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Posttraumatic stress disorder (PTSD) is associated with decreased activity in the dorsolateral prefrontal cortex (DLPFC), the brain region that regulates working memory and preparation and selection of fear responses. We investigated gene expression profiles in DLPFC Brodmann area (BA) 46 of postmortem patients with (n=6) and without PTSD (n=6) using human mitochondria-focused cDNA microarrays. Our study revealed PTSD-specific expression fingerprints of 800 informative mitochondria-focused genes across all of these 12 BA46 samples, and 119 (±>1.25, p<0.05) and 42 (±>1.60, p<0.05) dysregulated genes between the PTSD and control samples. Quantitative RT-PCR validated the microarray results. These fingerprints can essentially distinguish the PTSD DLPFC BA46 brains from controls. Of the 119 dysregulated genes (±≥125%, p<0.05), the highest percentages were associated with mitochondrial dysfunction (4.8%, p=6.61x10-6), oxidative phosphorylation (3.8%, p=9.04x10-4), cell survival-apoptosis (25.2%, p<0.05) and neurological diseases (23.5%, p<0.05). Fifty (50) dysregulated genes were present in the molecular networks that are known to be involved in neuronal function-survival and contain 7 targets for neuropsychiatric drugs. Thirty (30) of the dysregulated genes are associated with a number of neuropsychiatric disorders. Our results indicate mitochondrial dysfunction in the PTSD DLPFC BA46 and provide the expression fingerprints that may ultimately serve as biomarkers for PTSD diagnosis and the drugs and molecular targets that may prove useful for development of remedies for prevention and treatment of PTSD.

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“…The most prominent and persistent symptoms revealed in patients with PTSD are hypervigilance, delayed exaggerated startle response 14,15,16 and an apparent compromise of the HPA axis. In humans these symptoms remain, or appear with a delay of three months, after cessation of the traumatic stressor 24 . Our current model for biomarker studies of PTSD employs restraint and tail shocks repeated for three continuous days (2-hr sessions of 40, 2 mA tailshocks) -the inescapable tail-shock model (ITS) in rats weighing 150 gram.…”

Section: Discussionmentioning

confidence: 99%

Biomarkers in an Animal Model for Revealing Neural, Hematologic, and Behavioral Correlates of PTSD

Jia

Meng

Smerin

et al. 2012

JoVE

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Identification of biomarkers representing the evolution of the pathophysiology of Post Traumatic Stress Disorder (PTSD) is vitally important, not only for objective diagnosis but also for the evaluation of therapeutic efficacy and resilience to trauma. Ongoing research is directed at identifying molecular biomarkers for PTSD, including traumatic stress induced proteins, transcriptomes, genomic variances and genetic modulators, using biologic samples from subjects' blood, saliva, urine, and postmortem brain tissues. However, the correlation of these biomarker molecules in peripheral or postmortem samples to altered brain functions associated with psychiatric symptoms in PTSD remains unresolved. Here, we present an animal model of PTSD in which both peripheral blood and central brain biomarkers, as well as behavioral phenotype, can be collected and measured, thus providing the needed correlation of the central biomarkers of PTSD, which are mechanistic and pathognomonic but cannot be collected from people, with the peripheral biomarkers and behavioral phenotypes, which can.Our animal model of PTSD employs restraint and tail shocks repeated for three continuous days -the inescapable tail-shock model (ITS) in rats. This ITS model mimics the pathophysiology of PTSD 17, 7, 4, 10 . We and others have verified that the ITS model induces behavioral and neurobiological alterations similar to those found in PTSD subjects 17, 7, 10, 9 . Specifically, these stressed rats exhibit (1) a delayed and exaggerated startle response appearing several days after stressor cessation, which given the compressed time scale of the rat's life compared to a humans, corresponds to the one to three months delay of symptoms in PTSD patients (DSM-IV-TR PTSD Criterian D/E 13 ), (2) enhanced plasma corticosterone (CORT) for several days, indicating compromise of the hypothalamopituitary axis (HPA), and (3) retarded body weight gain after stressor cessation, indicating dysfunction of metabolic regulation.The experimental paradigms employed for this model are: (1) a learned helplessness paradigm in the rat assayed by measurement of acoustic startle response (ASR) and a charting of body mass; (2) microdissection of the rat brain into regions and nuclei; (3) enzyme-linked immunosorbent assay (ELISA) for blood levels of CORT; (4) a gene expression microarray plus related bioinformatics tools 18 . This microarray, dubbed rMNChip, focuses on mitochondrial and mitochondria-related nuclear genes in the rat so as to specifically address the neuronal bioenergetics hypothesized to be involved in PTSD. Video LinkThe video component of this article can be found at https://www.jove.com/video/3361/ Protocol 1. Animal Behavioral Model of PTSD 1. Subjects: Male albino Sprague Dawley rats (Taconic Farms, Derwood, MD) are used, weighting 150 to 200 g at the time of administration of the stress protocol. 2. Measurement of food, water intake and body weight gain: On arrival in the laboratory rats weighing 100 ± 25 g are housed two to a cage (cage size:...

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Molecular mechanism underlying differential apoptosis between human melanoma cell lines UACC903 and UACC903(+6) revealed by mitochondria-focused cDNA microarrays

Cited by 15 publications

References 40 publications

Downregulation of miR-125b in metastatic cutaneous malignant melanoma

Downregulation of miR-125b in metastatic cutaneous malignant melanoma

Dysregulated Mitochondrial Genes and Networks with Drug Targets in Postmortem Brain of Patients with Posttraumatic Stress Disorder (PTSD) Revealed by Human Mitochondria-Focused cDNA Microarrays

Biomarkers in an Animal Model for Revealing Neural, Hematologic, and Behavioral Correlates of PTSD

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