MicroRNA Profiling of Sporadic and Hereditary Medullary Thyroid Cancer Identifies Predictors of Nodal Metastasis, Prognosis, and Potential Therapeutic Targets

Abraham, Deepak Thomas; Jackson, Nicole; Gundara, Justin S.; Zhao, Jiuliang; Gill, Anthony J.; Delbridge, Leigh; Robinson, Bruce G.; Sidhu, Stan

doi:10.1158/1078-0432.ccr-11-0242

Cited by 129 publications

(129 citation statements)

References 34 publications

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“…In a series of 19 MTC, a signature of three miRNA (miR-183, miR-375, and miR-9*) enabled to distinguish familial from sporadic cases (Abraham et al 2011). Mian et al (2012) analyzed the expression of nine miRNA (miR-21, miR-127, miR-154, miR-224, miR-323, miR-370, miR-9*, miR-183, and miR-375) in 34 sporadic MTC and correlated this expression with RET status.…”

Section: Micrornamentioning

confidence: 99%

RAS proto-oncogene in medullary thyroid carcinoma

Moura¹,

Cavaco²,

Leite³

2015

Endocrine-Related Cancer

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Medullary thyroid carcinoma (MTC) is a rare malignancy originating from the calcitoninsecreting parafollicular thyroid C cells. Approximately 75% of cases are sporadic. Rearranged during transfection (RET) proto-oncogene plays a crucial role in MTC development. Besides RET, other oncogenes commonly involved in the pathogenesis of human cancers have also been investigated in MTC. The family of human RAS genes includes the highly homologous HRAS, KRAS, and NRAS genes that encode three distinct proteins. Activating mutations in specific hotspots of the RAS genes are found in about 30% of all human cancers. In thyroid neoplasias, RAS gene point mutations, mainly in NRAS, are detected in benign and malignant tumors arising from the follicular epithelium. However, recent reports have also described RAS mutations in MTC, namely in HRAS and KRAS. Overall, the prevalence of RAS mutations in sporadic MTC varies between 0-43.3%, occurring usually in tumors with WT RET and rarely in those harboring a RET mutation, suggesting that activation of these proto-oncogenes represents alternative genetic events in sporadic MTC tumorigenesis. Thus, the assessment of RAS mutation status can be useful to define therapeutic strategies in RET WT MTC. MTC patients with RAS mutations have an intermediate risk for aggressive cancer, between those with RET mutations in exons 15 and 16, which are associated with the worst prognosis, and cases with other RET mutations, which have the most indolent course of the disease. Recent results from exome sequencing indicate that, besides mutations in RET, HRAS, and KRAS, no other recurrent driver mutations are present in MTC.

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Section: Micrornamentioning

confidence: 99%

RAS proto-oncogene in medullary thyroid carcinoma

Moura¹,

Cavaco²,

Leite³

2015

Endocrine-Related Cancer

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“…PDTCs are medium carcinomas between WDTCs and ATCs. Medullary thyroid cancers (MTCs), the neuroendocrine tumor of the thyroid gland, are derived from parafollicular C cells (Pallante et al, 2010) and present as the hereditary form (HMTC; 25%) and the sporadic form (SMTC; 75%) (Abraham et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Deregulation of microRNA expression in thyroid tumors

Yuan

Yang

Zheng

2014

J. Zhejiang Univ. Sci. B

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MicroRNAs (miRNAs or miRs) are endogenous non-coding RNAs that negatively regulate gene expression by binding to the 3' non-coding regions of target mRNAs, resulting in their cleavage or blocking their translation. miRNAs may have an impact on cell differentiation, proliferation, and survival, and their deregulation can be inclined to diseases and cancers, including thyroid tumors. The purpose of this review is to summarize the existing findings of deregulated miRNAs in different types of thyroid tumors and to exhibit their potential target genes, especially to demonstrate those involved in tumor invasion and metastasis. In addition, new findings of circulating miRNA expression profiles, single nucleotide polymorphism (SNP) in thyroid tumors, and the correlation of somatic mutations with deregulated miRNA expression in thyroid tumors were all included in this review.

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“…Antagonizing miRNA-183 in an MTC cell line revealed a decrease in viable cancer cells in the absence of apoptosis marker changes, as well as a simultaneous increase in autophagy (Abraham et al 2011). This finding suggests, but does not prove, that autophagy is the cause of cell death.…”

Section: Autophagy In Thyroid Cancermentioning

confidence: 80%

“…The search for an effective treatment other than surgery for MTC has yielded another potential treatment target in microRNA-183, which is overexpressed in sporadic MTC (Abraham et al 2011). Antagonizing miRNA-183 in an MTC cell line revealed a decrease in viable cancer cells in the absence of apoptosis marker changes, as well as a simultaneous increase in autophagy (Abraham et al 2011).…”

Section: Autophagy In Thyroid Cancermentioning

confidence: 99%

“…As with most of the cases discussed here, it remains possible that autophagy is up-regulated as a survival attempt and that cell death occurs in spite of autophagy rather than because of it. In fact, another microRNA, miR-9-3p was shown to be down-regulated in sporadic MTC (Abraham et al 2011) and its transfection into MTC cell lines reduced cell viability, at least partially, via a decrease in autophagic flux and autophagy-related gene expression and a concurrent increase in apoptotic flux (Gundara et al 2015). Interestingly, Gundara et al (2015) also investigated the mRNA autophagy gene profile in clinical samples of both sporadic and hereditary MTC.…”

Section: Autophagy In Thyroid Cancermentioning

confidence: 99%

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Autophagy in endocrine tumors

Weckman¹,

Rotondo²,

Ieva³

et al. 2015

Endocrine-Related Cancer

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Autophagy is an important intracellular process involving the degradation of cytoplasmic components. It is involved in both physiological and pathological conditions, including cancer. The role of autophagy in cancer is described as a 'double-edged sword,' a term that reflects its known participation in tumor suppression, tumor survival and tumor cell proliferation. Available research regarding autophagy in endocrine cancer supports this concept. Autophagy shows promise as a novel therapeutic target in different types of endocrine cancer, inhibiting or increasing treatment efficacy in a context-and cell-typedependent manner. At present, however, there is very little research concerning autophagy in endocrine tumors. No research was reported connecting autophagy to some of the tumors of the endocrine glands such as the pancreas and ovary. This review aims to elucidate the roles of autophagy in different types of endocrine cancer and highlight the need for increased research in the field.

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MicroRNA Profiling of Sporadic and Hereditary Medullary Thyroid Cancer Identifies Predictors of Nodal Metastasis, Prognosis, and Potential Therapeutic Targets

Cited by 129 publications

References 34 publications

RAS proto-oncogene in medullary thyroid carcinoma

RAS proto-oncogene in medullary thyroid carcinoma

Deregulation of microRNA expression in thyroid tumors

Autophagy in endocrine tumors

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