scholarly journals DEHP Down-Regulates Tshr Gene Expression in Rat Thyroid Tissues and FRTL-5 Rat Thyrocytes: A Potential Mechanism of Thyroid Disruption

2021 ◽  
Author(s):  
Min Joo Kim ◽  
Hwan Hee Kim ◽  
Young Shin Song ◽  
Ok-Hee Kim ◽  
Kyungho Choi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Potential Mechanism ◽  
Thyroid Disruption ◽  
Tshr Gene ◽  
Rat Thyroid

scholarly journals Clinical implication of centrosome amplification in plasma cell neoplasm

Blood ◽  
2006 ◽  
Vol 107 (9) ◽  
pp. 3669-3675 ◽  
Author(s):  
Wee J. Chng ◽  
Greg J. Ahmann ◽  
Kim Henderson ◽  
Rafael Santana-Davila ◽  
Philip R. Greipp ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multivariate Regression ◽  
Monoclonal Gammopathy ◽  
Chromosomal Instability ◽  
Centrosome Amplification ◽  
Expression Data ◽  
Potential Mechanism ◽  
Plasma Cell Neoplasm ◽  
Cell Neoplasm ◽  
Undetermined Significance

The mechanisms underlying aneuploidy in multiple myeloma (MM) are unclear. Centrosome amplification has been implicated as the cause of chromosomal instability in a variety of tumors and is a potential mechanism causing aneuploidy in MM. Using immunofluorescent (IF) staining, centrosome amplification was detected in 67% of monoclonal gammopathies, including monoclonal gammopathy of undetermined significance (MGUS). We also investigated the gene expression of centrosome proteins. Overall, gene expression data correlated well with IF-detected centrosome amplification, allowing us to derive a gene expression-based centrosome index (CI) as a surrogate for centrosome amplification. Clinically, MM patients with high CI (> 4) are associated with poor prognostic genetic and clinical subtypes (chromosome 13 deletion, t(4; 14), t(14;16), and PCLI > 1%, P < .05) and are shown here to have short survival (11.1 months versus 39.1 months, P < .001). On multivariate regression, a high CI is an independent prognostic factor. Given that centrosome amplification is already observed in MGUS and probably integral to early chromosomal instability and myeloma genesis, and patients with more extensive centrosome amplification have shorter survival, the mechanisms leading to centrosome amplification should be investigated because these may offer new avenues for therapeutic intervention.

Induction of UCP2 Gene Expression by LPS: A Potential Mechanism for Increased Thermogenesis during Infection

1998 ◽  
Vol 244 (1) ◽  
pp. 75-78 ◽  
Author(s):  
Raffaella Faggioni ◽  
Judy Shigenaga ◽  
Arthur Moser ◽  
Kenneth R. Feingold ◽  
Carl Grunfeld
Keyword(s):  
Gene Expression ◽  
Potential Mechanism ◽  
Ucp2 Gene

Extinction and activation of the thyroglobulin promoter in hybrids of differentiated and transformed thyroid cells

1990 ◽  
Vol 10 (3) ◽  
pp. 1033-1040
Author(s):  
I M Bonapace ◽  
M Sanchez ◽  
S Obici ◽  
A Gallo ◽  
S Garofalo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Selectable Marker ◽  
Hybrid Cell ◽  
Transformed Cells ◽  
Thyroid Cells ◽  
Dominant Selectable Marker ◽  
Thyroglobulin Gene ◽  
Rat Thyroid ◽  
Hybrid Cell Lines

Thyroglobulin gene expression was repressed in a rat thyroid cell line transformed with Kirsten murine sarcoma virus. Expression of a dominant selectable marker driven by the thyroglobulin promoter was also inhibited. Somatic cell hybridization of transformed and differentiated thyroid cells resulted in extinction of thyroglobulin gene expression. When transformed cells carrying a dominant selectable marker driven by the thyroglobulin promoter were fused to differentiated cells and expression of this marker was selected, we obtained stable hybrid cell lines expressing both the endogenous and the exogenous thyroglobulin promoters. Although the expression of v-ras remained unchanged compared with expression in the parental transformed cells, transformation was suppressed in the hybrid cell lines. The other thyroid differentiation markers, iodide uptake and thyroid-stimulating hormone-dependent growth, were inhibited in all the hybrids tested. We show that activity of the thyroglobulin promoter correlates with the presence of a thyroid nuclear factor that binds the promoter at position -60 from the transcription start site. Loss of this factor accompanies the extinction of thyroglobulin gene expression in hybrids selected for expression of a non-thyroid-specific promoter.

scholarly journals MicroRNAs in Female Malignancies

2019 ◽  
Vol 18 ◽  
pp. 117693511982874 ◽  
Author(s):  
Themis Liolios ◽  
Stavroula Lila Kastora ◽  
Giorgia Colombo
Keyword(s):  
Gene Expression ◽  
Computational Analysis ◽  
Target Genes ◽  
Vulvar Cancer ◽  
Chemotherapeutic Agents ◽  
In Vitro Assays ◽  
Biological Processes ◽  
Potential Mechanism ◽  
Biological Functions

MicroRNAs (miRNAs) are endogenous 22-nucleotide RNAs that can play a fundamental regulatory role in the gene expression of various organisms. Current research suggests that miRNAs can assume pivotal roles in carcinogenesis. In this article, through bioinformatics mining and computational analysis, we determine a single miRNA commonly involved in the development of breast, cervical, endometrial, ovarian, and vulvar cancer, whereas we underline the existence of 7 more miRNAs common in all examined malignancies with the exception of vulvar cancer. Furthermore, we identify their target genes and encoded biological functions. We also analyze common biological processes on which all of the identified miRNAs act and we suggest a potential mechanism of action. In addition, we analyze exclusive miRNAs among the examined malignancies and bioinformatically explore their functionality. Collectively, our data can be employed in in vitro assays as a stepping stone in the identification of a universal machinery that is derailed in female malignancies, whereas exclusive miRNAs may be employed as putative targets for future chemotherapeutic agents or cancer-specific biomarkers.

scholarly journals Overexpression of thyroid hormone receptor beta1 is associated with thyrotropin receptor gene expression and proliferation in a human thyroid carcinoma cell line

2000 ◽  
Vol 165 (2) ◽  
pp. 379-389 ◽  
Author(s):  
ST Chen ◽  
HY Shieh ◽  
JD Lin ◽  
KS Chang ◽  
KH Lin
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Thyroid Hormone ◽  
Cell Line ◽  
Cell Lines ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Human Thyroid ◽  
Thyrotropin Receptor ◽  
Tshr Gene

To correlate the differentiation phenotype of two human thyroid cancer cell lines with their expression of various molecular markers, we analyzed the mRNA levels of four thyroid-specific genes, including thyrotropin receptor (TSHR), thyroglobulin (Tg), thyroid transcription factor-1 (TTF-1), and paired-box containing transcription factor-8 (PAX-8) genes. The results showed a differentiation-status-related pattern in which a well-differentiated cell line (WRO) expressed all the four genes, in contrast to an anaplastic cell line (ARO) that expressed TTF-1 and reduced levels of TSHR, but no Tg or PAX-8 genes. Furthermore, to verify the finding of concomitant loss of beta subtype thyroid hormone receptor (TRbeta) and TSHR gene expression in neoplastic thyroid tumors (Bronnegard et al. 1994), we examined the expression levels of TRbeta1 gene in these cell lines. Whereas the WRO cells produced an abundant amount of TRbeta1 protein detectable by immunoprecipitation, the ARO cells produced none. This new observation prompted us to investigate whether overexpression of TRbeta1 protein in ARO cells might produce changes in the differentiation phenotypes. We found that the level of expression of the TSHR gene and the proliferative index of ARO cells were significantly upregulated in the cells stably transfected with wild-type TRbeta1. These findings suggest that TRbeta1 protein overexpression can affect the differentiation phenotypes and induce more efficient cell proliferation of the anaplastic ARO cells.

Disrupted co-ordination of Pax-8 and thyroid transcription factor-1 gene expression in a dedifferentiated rat thyroid tumour cell line derived from FRTL-5

1996 ◽  
Vol 150 (3) ◽  
pp. 377-382 ◽  
Author(s):  
C J H van der Kallen ◽  
D C J Spierings ◽  
J H H Thijssen ◽  
M A Blankenstein ◽  
T W A de Bruin
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Cell Line ◽  
Thyroid Peroxidase ◽  
Wild Type ◽  
Specific Expression ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Rat Thyroid ◽  
Transcription Factor 1

Abstract The mutant rat thyroid cell line FRTL-5/TA, isolated from a non-functional tumour which originated spontaneously from wild-type FRTL-5 cells, shows autonomous TSH-independent growth and loss of the thyroid-specific phenotype, lacking thyroid-specific expression of thyroglobulin (Tg) and thyroid peroxidase (TPO) genes. To investigate the role of the transcription factors Pax-8 and thyroid transcription factor-1 (TTF-1) in rat thyroid tumorigenesis, RNA expression of these two thyroid-specific nuclear factors was measured in FRTL-5/TA tumour cells and compared with the expression in wild-type FRTL-5 cells. TTF-1 gene expression was similar to that in wild-type FRTL-5, and showed a similar down-regulation after stimulation with TSH. The finding suggested normal TTF-1 mRNA and protein expression in both cell lines. By contrast, Pax-8 mRNA transcript signal was markedly reduced in FRTL-5/TA cells, reaching levels as low as 8% of the normal, basal level in FRTL-5 cells. These data indicated that the loss of thyroid-specific expression of Tg and TPO genes in FRTL-5/TA cells was not related to changes in TTF-1 gene expression but rather to reduced Pax-8 gene expression. It was concluded that a disruption of the co-ordinated expression of TTF-1 and Pax-8 is implicated in the loss of thyroid phenotype of FRTL-5/TA cells in terms of reduced Tg and TPO expression. Journal of Endocrinology (1996) 150, 377–382

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