Proteomic Profiling of Thyroid Papillary Carcinoma

Ban, Yoshiyuki; Yamamoto, Gou; Takada, Michiya; Hayashi, Shigeo; Ban, Yoshio; Shimizu, Kazuo; Akasu, Haruki; Igarashi, Takehito; Bando, Yoshio; Tachikawa, Tetsuhiko; Hirano, Tsutomu

doi:10.1155/2012/815079

Cited by 16 publications

(19 citation statements)

References 21 publications

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“…Together, these data are consistent with a model in which miR-26a suppresses CKS2 expression, leading to suppressed of cyclin B1 and cdk1 expression and G 2 arrested, similar to the findings of a previous study [15]. Moreover, consistent with the previous data [16], our results indicate that miR-26a induced cell apoptosis involves by Bcl-xl and Akt, which are mainly involved in programmed cell death.…”

Section: Discussionsupporting

confidence: 93%

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miR-26a and its Target CKS2 Modulate Cell Growth and Tumorigenesis of Papillary Thyroid Carcinoma

Zhang

et al. 2013

PLoS ONE

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BackgroundWhile many studies have shown that levels of miR-26a are lower in papillary thyroid carcinoma (PTC), the role and mechanism of miR-26a in PTC are unclear.MethodWe used database searches to select potential mRNA targets of miR-26a. Anti-miR-26a, miR-26a mimic, siRNA for CKS2 and their effects on cell growth, cell-cycle distribution and colony formation were evaluated. We also evaluate the over-expressed miR-26a in TPC-1 cells in severe combined immune-deficient mice. We used luciferase reporter assays, real-time PCR and western blot analysis to measure the expression and activity of miR-26a, CKS2, and related factors such as cyclin B1, cyclin A, cdk1, bcl-xl and Akt. Finally, we measured the relationship between the levels of miR-26a and CKS2 in PTC and normal thyroid tissues.ResultsRelative to normal thyroid tissues, miR-26a is consistently down-regulated in TPC specimens, and CKS2 was identified as a potential target. Up-regulated miR-26a expression or down-regulated CKS2 expression in TPC-1 and CGTH W3 cells lines caused G2 phase-arrest. Decreased miR-26a expression or increased CKS2 expression could have inverse function on PTC cell lines. CyclinB1, cyclinA, bcl-xl and AKt are indirectly regulated by miR-26a in a CKS2-dependent manner. Finally, CKS2 is overexpressed in PTC specimens relative to normal thyroid tissue, and a significant inverse correlation exists between miR-26a and CKS2 expression in clinical PTC specimens.ConclusionOur data indicate that miR-26a functions as a growth-suppressive miRNA in PTC, and that its suppressive effects are mediated mainly by repressing CKS2 expression.

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Section: Discussionsupporting

confidence: 93%

“…PTC is the most common form of follicular-cell derived carcinomas and comprises 75% of all newly-diagnosed thyroid cancers [16]. While studies have shown that miR-26a is down-regulated in PTC [4], [5], [6], [7], [8], to date no data have been available regarding the mechanism of miR-26a in this disease.…”

Section: Discussionmentioning

confidence: 99%

miR-26a and its Target CKS2 Modulate Cell Growth and Tumorigenesis of Papillary Thyroid Carcinoma

Zhang

et al. 2013

PLoS ONE

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“…In particular, studies of the thyrocyte and thyroid cancer proteomics, both ex vivo [26][27][28][29] and of cell lines [25] are in a minority compared with studies of the genome and transcriptome [30,31].…”

Section: Discussionmentioning

confidence: 99%

Differential proteomic and phenotypic behaviour of papillary and anaplastic thyroid cell lines

Musso

Cara

Albanese

et al. 2013

Journal of Proteomics

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Thyroid carcinomas account for a minority of all malignant tumours but, after those of the gonads, they represent the most common forms of endocrine cancers. They include several types, among which the papillary thyroid cancer (PTC) and the anaplastic thyroid cancer (ATC) are the best known. The two hystotypes display significant biological and clinical differences: PTC is a well differentiated form of tumour with a high incidence and a good prognosis, while the ATC is less frequent but represents one of the most aggressive endocrine tumours with morphological features of an undifferentiated type. To date, as far as we know, no conclusive studies, useful to design arrays of molecular markers, have been published illustrating the phenotypic and proteomic differences between these two tumours. The aim of this work was to perform a comparative analysis of two thyroid cancer cell lines, derived respectively from papillary (BCPAP) and anaplastic (8505C) thyroid carcinomas. The comparative analysis included cell behaviour assays and proteomic analysis by 2D-PAGE and mass spectrometry. IntroductionThe human thyroid gland is composed of a basic structural unit, the follicle, consisting of a monolayer of well polarized cells, the thyrocytes, responsible for the T3/T4 hormone secretion, and of other peripheral cells, the parafollicular C cells, responsible for the secretion of calcitonin. The presence within the follicle of stem cells, or remnants of embryonic cells, has been hypothesized as the target cells for tumour initiation. A thin extracellular matrix, which includes occasional fibroblasts and inflammatory cells, is peripheral to the follicle structure. Thyroid carcinomas account for 1-2% of all malignant tumours and, after those of the gonads, they represent the most common tumours of the endocrine system. The thyroid

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“…MLEC is an endoplasmic reticulum-resident lectin participating in the identification and degradation of misfolding glycoproteins. Overexpression of MLEC was considered as one of the new markers in papillary thyroid carcinoma (Ban et al, 2012). Downregulation of hsa-miR-133a-3p has already been determined as a selective marker in colon cancer (Weber et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Post-Transcriptional Dysregulation of microRNA and Alternative Polyadenylation in Colorectal Cancer

et al. 2020

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Background: Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide. microRNAs (miRNAs) repress gene expression by binding to complementary sequences in the 3' untranslated region (3'UTR) of target mRNAs. Alternative polyadenylation (APA) are relevant to the variability of the 3'UTR of mRNA. However, the posttranscriptional dysregulation of miRNAs and APA in CRC are poorly understood.Method: In this study, we conducted small RNA sequencing to identify differentially expressed miRNAs (DERs) and their target genes. Function analysis on DER-target genes can explain the regulation roles of miRNAs in CRC. The mutual regulation of miRNAs and APA was analyzed by combining miRNA data to 3'UTR alteration using 3' termini of polyadenylated RNAs sequencing (3T-seq) technique, and this was validated using TCGA gene expression data.Results: Our results showed 64 significant differentially expressed miRNAs (DERs) in CRC patients. Their target genes were related to cell adhesion and transcription regulation and were prevailingly involved in the CRC-related pathway. Integrative analysis of the miRNA and APA profile revealed 16 DERs were correlated with 12 polyadenylation factors, and six of them were significantly differently expressed in CRC. We also found four DERs that lost binding sites due to APA and showed a positive correlation between the miRNA and gene expression.Conclusion: Our study found that miRNAs regulated APA by modulating key polyadenylation factors, and several miRNAs lost their suppression on mRNA due to APA. Associating this with gene expression may provide some important clues for a deeper study of posttranscriptional cellular regulation and biomarker research in CRC. Our data provided the first evidence that the interaction between miRNAs and APA associated with gene expression could serve as biomarkers for CRC, suggesting that hsa-miR-133a-Frontiers in Genetics | www.frontiersin.org 3p and MLEC, hsa-miR-145-5p and SET, hsa-miR-1-3p and PPIA, and hsa-miR-378d and YY1 might be novel and potential biomarkers in improving the diagnosis of CRC.

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Proteomic Profiling of Thyroid Papillary Carcinoma

Cited by 16 publications

References 21 publications

miR-26a and its Target CKS2 Modulate Cell Growth and Tumorigenesis of Papillary Thyroid Carcinoma

miR-26a and its Target CKS2 Modulate Cell Growth and Tumorigenesis of Papillary Thyroid Carcinoma

Differential proteomic and phenotypic behaviour of papillary and anaplastic thyroid cell lines

Post-Transcriptional Dysregulation of microRNA and Alternative Polyadenylation in Colorectal Cancer

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