Thyroid Tumor: Investigating MicroRNA-21 Gene Suppression in FTC and FTA

Nwadiugwu, Martin C

doi:10.1177/1176935120948474

Cited by 6 publications

(7 citation statements)

References 53 publications

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“…The upregulation of miR-21 has also been reported in thyroid cancers, including PTC, FTC, and medullary thyroid carcinoma. It is correlated with tumor aggressiveness and advanced cancer stage [13,17,28,29]. The expression of miR-21 is regulated by DNA methylation in PTC [30].…”

Section: Discussionmentioning

confidence: 99%

“…Target genes of miR-21 include phosphatase and tensin homolog (PTEN), thyroid hormone receptor beta (THRB), programmed cell death 4 (PDCD4), B-cell lymphoma 2 (BCL2), and cell division cycle 25A (CDC25A) genes [13]. A recent study showed that the overexpression of miR-21-3p and miR-21-5p in FTC and FA downregulated the expression of tumor suppressor genes, such as metalloproteinase-3 (TIMP3), methionine adenosyltransferase 2 (MAT2A), transforming growth factor beta receptor II (TGFBR2), and plasminogen activator (PLAT) genes [29].…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA Profile for Diagnostic and Prognostic Biomarkers in Thyroid Cancer

Park

Kim

Jeon

et al. 2021

Cancers

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The challenge in managing thyroid nodules is to accurately diagnose the minority of those with malignancy. We aimed to identify diagnostic and prognostic miRNA markers for thyroid nodules. In a discovery cohort, we identified 20 candidate miRNAs to differentiate between noninvasive follicular thyroid neoplasms with papillary-like nuclear features (NIFTP) and papillary thyroid carcinomas (PTC) by using the high-throughput small RNA sequencing method. We then selected three miRNAs (miR-136, miR-21, and miR-127) that were differentially expressed between the PTC follicular variant and other variants in The Cancer Genome Atlas data. High expression of three miRNAs differentiated thyroid cancer from nonmalignant tumors, with an area under curve (AUC) of 0.76–0.81 in an independent cohort. In patients with differentiated thyroid cancer, the high-level expression of the three miRNAs was an independent indicator for both distant metastases and recurrent or persistent disease. In patients with PTC, a high expression of miRNAs was associated with an aggressive histologic variant, extrathyroidal extension, distant metastasis, or recurrent or persistent disease. Three miRNAs may be used as diagnostic markers for differentiating thyroid cancers from benign tumors and tumors with extremely low malignant potential (NIFTP), as well as prognostic markers for predicting the risk of recurrent/persistent disease for differentiated thyroid cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA Profile for Diagnostic and Prognostic Biomarkers in Thyroid Cancer

Park

Kim

Jeon

et al. 2021

Cancers

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“…It is important to know the role Adh6-ps1 interactions with MirRNAs play in gene regulation because MirRNAs are vital in investigating genes for possible involvement in tumorigenesis, apoptosis, pathogenesis, and disease resistance. 21 …”

Section: Resultsmentioning

confidence: 99%

Expression, Interaction, and Role of Pseudogene Adh6-ps1 in Cancer and other Disease Phenotypes

Nwadiugwu

2021

Bioinform Biol Insights

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Pseudogenes have been classified as functionless and their annotation is an ongoing problem. The Adh6-ps1—a mouse pseudogene belonging to the alcohol dehydrogenase gene complex (Adh) was analyzed to review the conservation, homology, expression, and interactions and identify any role it plays in disease phenotypes using bioinformatics databases. Results showed that Adh6-ps1 have 2 transcripts (processed and unprocessed) which may have emerged from a transposition and duplication event, respectively, and that induced inversions (Uox gene, In(3)11Rk) involving gene complexes associated with Adh6-ps1 have been implicated in a diverse range of diseases. Adh6-ps1 is highly conserved in vertebrates particularly rodents and expressed in the liver. The top 5 MirRNA targets were Mir455, Mir511, Mir1903, Mir361, and Mir669o markers. While much is unknown about Mir1903 and Mir669o, the silencing of Mir455 and Mir511 is linked with hepatocellular carcinoma (HCC), and Mir361 is implicated in endometrial cancers. Given the identified MirRNA interactions with Adh6-ps1 and its expression in HCC and reproductive systems, it may well have a role in tumorigenesis and disease phenotypes. Nonetheless, further studies are required to establish these facts to add to the growing efforts to understand pseudogenes and their potential involvement in disease conditions.

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“…Such features regarding miR-21 activity were never investigated in hepatic cancers. As well, in thyroid cancer, although an oncogenic role for miR-21 was suggested [ 103 ], others reported that miR-21 was not located in the active counterpart of the RNA-induced silencing complex (RISC) [ 104 , 105 ], indicating that despite its overexpression, miR-21 is inactive in this cancer. In MCF-7 cells also, miR-21 was shown to be sequestered by the RNA-binding protein HuR, thereby preventing mRNA decay of PDCD4 , a classical target of miR-21 [ 93 ].…”

Section: Discussionmentioning

confidence: 99%

Mir-21 Suppression Promotes Mouse Hepatocarcinogenesis

Sousa

Calo

Sobolewski

et al. 2021

Cancers

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The microRNA 21 (miR-21) is upregulated in almost all known human cancers and is considered a highly potent oncogene and potential therapeutic target for cancer treatment. In the liver, miR-21 was reported to promote hepatic steatosis and inflammation, but whether miR-21 also drives hepatocarcinogenesis remains poorly investigated in vivo. Here we show using both carcinogen (Diethylnitrosamine, DEN) or genetically (PTEN deficiency)-induced mouse models of hepatocellular carcinoma (HCC), total or hepatocyte-specific genetic deletion of this microRNA fosters HCC development—contrasting the expected oncogenic role of miR-21. Gene and protein expression analyses of mouse liver tissues further indicate that total or hepatocyte-specific miR-21 deficiency is associated with an increased expression of oncogenes such as Cdc25a, subtle deregulations of the MAPK, HiPPO, and STAT3 signaling pathways, as well as alterations of the inflammatory/immune anti-tumoral responses in the liver. Together, our data show that miR-21 deficiency promotes a pro-tumoral microenvironment, which over time fosters HCC development via pleiotropic and complex mechanisms. These results question the current dogma of miR-21 being a potent oncomiR in the liver and call for cautiousness when considering miR-21 inhibition for therapeutic purposes in HCC.

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Thyroid Tumor: Investigating MicroRNA-21 Gene Suppression in FTC and FTA

Cited by 6 publications

References 53 publications

MicroRNA Profile for Diagnostic and Prognostic Biomarkers in Thyroid Cancer

MicroRNA Profile for Diagnostic and Prognostic Biomarkers in Thyroid Cancer

Expression, Interaction, and Role of Pseudogene Adh6-ps1 in Cancer and other Disease Phenotypes

Mir-21 Suppression Promotes Mouse Hepatocarcinogenesis

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