Genetic alterations in oral squamous cell carcinoma progression detected by combining array-based comparative genomic hybridization and multiplex ligation-dependent probe amplification

Dan, Jeong; Kim, Hyung Jun; Ho, In

doi:10.1016/j.tripleo.2010.11.020

Cited by 39 publications

(27 citation statements)

References 52 publications

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“…As with transgelin, stromal PDLIM5 expression was unrelated to clinicopathologic parameters or survival in non-small cell lung carcinoma [46]. It was additionally shown to be deleted in oral squamous cell carcinoma by comparative genomic hybridization [48]. …”

Section: Discussionmentioning

confidence: 99%

Gene expression signatures differentiate uterine endometrial stromal sarcoma from leiomyosarcoma

Davidson

Abeler

Hellesylt

et al. 2013

Gynecologic Oncology

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Objective Endometrial stromal sarcoma (ESS) and leiomyosarcoma (LMS) are the two most common uterine sarcomas, but both are rare tumors. The aim of the present study was to compare the global gene expression patterns of ESS and LMS. Methods Gene expression profiles of 7 ESS and 13 LMS were analyzed using the HumanRef-8 BeadChip from Illumina. Differentially expressed candidate genes were validated using quantitative real-time PCR and immunohistochemistry. Results Unsupervised hierarchical clustering using all 54,675 genes in the array separated ESS from LMS samples. We identified 549 unique probes that were significantly differentially expressed in the two malignancies by greater than 2-fold with 1% FDR cutoff using one-way ANOVA with Benjamini–Hochberg correction, of which 336 and 213 were overexpressed in ESS and LMS, respectively. Genes overexpressed in ESS included SLC7A10, EFNB3, CCND2, ECEL1, ITM2A, NPW, PLAG1 and GCGR. Genes overexpressed in LMS included CDKN2A, FABP3, TAGLN, JPH2, GEM, NAV2 and RAB23. The top 100 genes overexpressed in LMS included those coding for myosin light chain and caldesmon, but not the genes coding for desmin or actin. CD10 was not overexpressed in ESS. Results for selected genes were validated by quantitative real-time PCR and immunohistochemistry. Conclusions We present the first study in which gene expression profiling was shown to distinguish between ESS and LMS. The molecular signatures unique to each of these malignancies may aid in expanding the diagnostic battery for their differentiation, and may provide a molecular basis for prognostic studies and therapeutic target discovery.

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Section: Discussionmentioning

confidence: 99%

Gene expression signatures differentiate uterine endometrial stromal sarcoma from leiomyosarcoma

Davidson

Abeler

Hellesylt

et al. 2013

Gynecologic Oncology

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“…In non-NDD diagnoses, overexpression of BRINP2 (FAM5b) or BRINP3 (FAM5c) has been implicated in cancer: BRINP2 is amplified in oral squamous cell carcinoma (Cha et al, 2011), and BRINP3 is overexpressed in pituitary adenomas (Shorts-Cary et al, 2007). Both genes also show association with coronary heart disease (Connelly et al, 2008; Angelakopoulou et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Mice Lacking Brinp2 or Brinp3, or Both, Exhibit Behaviors Consistent with Neurodevelopmental Disorders

Berkowicz

Featherby

Whisstock

et al. 2016

Front. Behav. Neurosci.

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Background: Brinps 1–3, and Astrotactins (Astn) 1 and 2, are members of the Membrane Attack Complex/Perforin (MACPF) superfamily that are predominantly expressed in the mammalian brain during development. Genetic variation at the human BRINP2/ASTN1 and BRINP1/ASTN2 loci has been implicated in neurodevelopmental disorders. We, and others, have previously shown that Brinp1−/− mice exhibit behavior reminiscent of autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD).Method: We created Brinp2−/− mice and Brinp3−/− mice via the Cre-mediated LoxP system to investigate the effect of gene deletion on anatomy and behavior. Additionally, Brinp2−/−Brinp3−/− double knock-out mice were generated by interbreeding Brinp2−/− and Brinp3−/− mice. Genomic validation was carried out for each knock-out line, followed by histological, weight and behavioral examination. Brinp1−/−Brinp2−/−Brinp3−/− triple knock-out mice were also generated by crossing Brinp2/3 double knock-out mice with previously generated Brinp1−/− mice, and examined by weight and histological analysis.Results: Brinp2−/− and Brinp3−/− mice differ in their behavior: Brinp2−/− mice are hyperactive, whereas Brinp3−/− mice exhibit marked changes in anxiety-response on the elevated plus maze. Brinp3−/− mice also show evidence of altered sociability. Both Brinp2−/− and Brinp3−/− mice have normal short-term memory, olfactory responses, pre-pulse inhibition, and motor learning. The double knock-out mice show behaviors of Brinp2−/− and Brinp3−/− mice, without evidence of new or exacerbated phenotypes.Conclusion: Brinp3 is important in moderation of anxiety, with potential relevance to anxiety disorders. Brinp2 dysfunction resulting in hyperactivity may be relevant to the association of ADHD with chromosome locus 1q25.2. Brinp2−/− and Brinp3−/− genes do not compensate in the mammalian brain and likely have distinct molecular or cell-type specific functions.

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“…As expected, according to our previous report on other human oral SCC-derived cell lines5, the current series of target molecules, i.e., HTR2C , Lin-7C , CASK (also known as Lin-2 ), and β-catenin , had steady-state levels of mRNAs in the SAS cells, whereas SAS-H1 had significantly lower expression levels. These molecules, especially for β-catenin , are critical factors in human carcinogenesis1011. In addition to Lin-7C, CASK is a cellular adhesion molecule with PDZ domains and thus can bind to the cellular surface1112, indicating that there may be a relationship between CASK and cellular metastasis/invasion.…”

Section: Discussionmentioning

confidence: 99%

“…Several reports have shown that CASK may affect epidermal adhesion and wound healing together with cellular migration, indicating a potential clue1314. In contrast, HTR2C seems to be altered in patients with oral SCC10, but the critical mechanism of human tumorigenesis remains inconclusive.…”

Section: Discussionmentioning

confidence: 99%

Suppression of metastasis by mirtazapine via restoration of the Lin-7C/β-catenin pathway in human cancer cells

Uzawa

Kasamatsu

Shimizu

et al. 2014

Sci Rep

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No definitive therapy exists to treat human metastatic tumors. We reported previously that down-regulation of Lin-7C is essential for metastasis of human squamous cell carcinomas (hSCCs). In this study, we investigated the chemical restoration of Lin-7C expression and demonstrated its effectiveness for suppressing the metastatic potential in human cancer cells. Ingenuity Pathway Analysis (IPA) identified candidate chemical agents, i.e., apomorphine, caffeine, risperidone, quetiapine, and mirtazapine. Among them, mirtazapine, an antagonist of HTR2C, an upstream molecule of Lin-7C, caused substantial up-regulation of the Lin-7C/β-catenin pathway in a metastatic hSCC cell line and human melanoma-derived cell line in vitro, and up-regulation did not contribute to cellular proliferation. Moreover, the antimetastatic effect of mirtazapine in these metastatic cell lines in vivo also was evident in multiple organs of immunodeficient mice with no marked side effects. The current data offer novel information for further study of antimetastatic activity in association with enhanced Lin-7C/β-catenin pathway activation with mirtazapine.

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Genetic alterations in oral squamous cell carcinoma progression detected by combining array-based comparative genomic hybridization and multiplex ligation-dependent probe amplification

Cited by 39 publications

References 52 publications

Gene expression signatures differentiate uterine endometrial stromal sarcoma from leiomyosarcoma

Gene expression signatures differentiate uterine endometrial stromal sarcoma from leiomyosarcoma

Mice Lacking Brinp2 or Brinp3, or Both, Exhibit Behaviors Consistent with Neurodevelopmental Disorders

Suppression of metastasis by mirtazapine via restoration of the Lin-7C/β-catenin pathway in human cancer cells

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