miR-29a-3p inhibits growth, proliferation, and invasion of papillary thyroid carcinoma by suppressing NF-&amp;kappa;B signaling via direct targeting of OTUB2

Ma, Yuju; Sun, Yu

doi:10.2147/cmar.s184781

Cited by 44 publications

(35 citation statements)

References 35 publications

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“…For example, miR-202-3p was found to be downregulated in PTC tissues, and to repress cell migra- tion as well as invasion in PTC [29]. Furthermore, enforced expression of miR-29a-3p could reduce cell growth, proliferation, and invasion in PTC [30]. Additionally, miR-128 was reported to be associated with the development of PTC and it could suppress the growth of PTC [31].…”

Section: Discussionmentioning

confidence: 99%

miR-326 inhibits the progression of papillary thyroid carcinoma by targeting MAPK1 and ERBB4

Nie

Wei

et al. 2020

neo

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Papillary thyroid carcinoma (PTC) is the prevalent histotype of thyroid cancer, with increasing incidence worldwide. MicroRNAs (miRNAs) could play an important role in the development and progression of human cancers. Interestingly, miR-326 was validated as one of the downregulated miRNAs in PTC. Therefore, it is necessary to research the function of miR-326 involved in the progression of PTC. In the current study, we detected the downregulation of miR-326 in PTC tissues and cell lines. The miR-326 overexpression or knockdown was conducted in TPC-1 or HTh83 PTC cells. miR-326 mimics decreased the proliferation, clone formation ability and caused G1-phase accumulation. In addition, the reduction of migration and invasion abilities was induced by miR-326 mimics. Western blot analysis showed that the cells with miR-326 mimics exhibited the inhibition of vimentin and N-cadherin, as well as enhancement of E-cadherin. Importantly, miR-326 could directly target mitogen activated protein kinase 1 (MAPK1) and epidermal growth factor receptor 4 (ERBB4). MAPK1 or ERBB4 overexpression rescued the effects of miR-326 on proliferation, migration, and invasion in PTC cells. Notably, miR-326 reduced tumorigenesis in vivo, including the decrease of tumor volume and weight, suppression of Ki-67, N-cadherin, MAPK1 and ERBB4. In all, these results might provide a new therapeutic target for the diagnosis of PTC.

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Section: Discussionmentioning

confidence: 99%

miR-326 inhibits the progression of papillary thyroid carcinoma by targeting MAPK1 and ERBB4

Nie

Wei

et al. 2020

neo

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“…MiR-16-5p was reportedly downregulated in breast cancer [76], hepatocellular carcinoma [77] and glioma [78], in agreement with our ndings. Overall, miR-29a-3p has been reported to function as a tumour suppressor and is downregulated in many types of cancers, such as thyroid carcinoma [32], colorectal carcinoma [79] and hepatocellular carcinoma [80].The downregulation of miR-34c-5p has been reported in several types of cancer, such as leukaemia [57] and osteosarcoma [58], and it has been closely associated with poor prognosis. Similarly, miR-490-5p is markedly downregulated in hepatocellular carcinoma tissues [81], in renal cell carcinoma tissues and cells [82] and in childhood neuroblastomas and cell lines [83].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-29a-3p is a potential tumour-suppressive miRNA and is downregulated in several cancer tissues, such as papillary thyroid carcinoma tissues and cell lines [32],hepatocellular carcinoma tissues and cell lines [33], gastric cancer tissues [34] and high-grade glioma tissues [35]. More studies have been conducted on miR-29a-3p than on miR-656-3p, miR-337-5p or miR-655-3p, and studies on exosomederived miR-29a-3p are very rare.…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression profiles and bioinformatic analysis of CAF-derived exosomal miRNAs from three moderately differentiated supraglottic LSCC patients

Wang

Huang

et al. 2020

Preprint

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Background Aberrant expression of exosomal miRNAs has emerged as a research hotspot in cancer studies. However, no studies have been conducted on the dysregulation of exosomal miRNAs derived from cancer-associated fibroblasts (CAFs) in supraglottic laryngeal squamous cell carcinoma (SLSCC). Methods CAFs and paired normal fibroblasts (NFs) from SLSCC patients were cultured, and exosomes in the culture supernatants were collected and identified by transmission electron microscopy, nanoparticle tracking analysis and western blotting. Exosomal miRNA expression was compared in each pair of CAFs and NFs by next-generation sequencing. Four online bioinformatic algorithms predicted the potential target genes of aberrantly expressed miRNAs, while gene ontology and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment and network analysis identified downstream target genes and their interactions. Results Three pairs of CAFs and NFs were successfully cultured and purified. CAF-derived exosomal miRNAs were mostly downregulated and included miR-656-3p, miR-337-5p, miR-29a-3p and miR-655-3p; however, some, including miR-184-3p, miR-92a-1-5p, miR-212-3p and miR-3135b, were upregulated. Bioinformatics analysis revealed involvement of these miRNAs in biological processes, cellular components and molecular functions. KEGG analysis revealed the top thirty pathways involvement in cancer initiation and progression and in cell cycle regulation. An interaction network showed miR-16-5p, miR-29a-3p, miR-34c-5p, miR-32-5p and miR-490-5p as the top five miRNAs and CCND1, CDKN1B, CDK6, PTEN and FOS as the top five target genes. Conclusions SLSCC patients showed aberrant expression of CAF-derived exosomal miRNAs. The target genes may jointly constitute a carcinogenic tumour microenvironment and may play decisive roles in the initiation and progression of SLSCC.

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“…Among them, Afmid has been reported that they could lead to impaired glucose tolerance in type 2 diabetes [36]. Meanwhile, Otub2 has been shown to act through the inhibition of NF-κB signaling in type 1 diabetes [37,38]. Further experiments should be performed to explore the precise regulatory relationship between these candidate mRNAs and lncRNA TCONS_00230836 as well as PERK/eIF2α-dependent signaling in stearic acid-treated β cells.…”

Section: Discussionmentioning

confidence: 99%

TCONS_00230836 silencing restores stearic acid-induced β-cell dysfunction through alleviating endoplasmic reticulum stress via a PERK/eIF2α-dependent pathway rather than apoptosis

Guo¹,

Zhang²,

Yu³

et al. 2020

Preprint

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Background: Chronic exposure of pancreatic β cells to high levels of stearic acid (C18:0) leads to impaired insulin secretion, which accelerates the progression of type 2 diabetes mellitus (T2DM). Recently, long noncoding RNAs (lncRNAs) were found to participate in saturated fatty acid-induced metabolism dysfunction. However, their contribution to stearic acid-induced β-cell dysfunction remains largely unknown. This study evaluated the possible role of the lncRNA TCONS_00230836 in stearic acid-stimulated lipotoxicity to β cells. Method: Using high-throughput RNA-sequencing, TCONS_00230836 was screened out as being exclusively differentially expressed in stearic acid-treated mouse β-TC6 cells. Co-expression network was constructed to reveal the potential mRNAs targeted for lncRNA TCONS_00230836. Changes in this lncRNA’s and candidate mRNAs’levels were further assessed by real-time PCR in stearic acid-treated β-TC6 cells and islets of mice fed a high-stearic-acid diet (HSD). The localization of TCONS_00230836 was detected by fluorescent in situ hybridization. The endogenous lncRNA TCONS_00230836 in β-TC6 cells was abrogated by its Smart Silencer. Results: The lncRNA TCONS_00230836 was enriched in mouse islets and mainly localized in the cytoplasm. Its expression was significantly increased in stearic acid-treated β-TC6 cells and HSD-fed mouse islets. Knockdown of TCONS_00230836 apparently restored stearic acid-impaired GSIS through alleviating endoplasmic reticulum stress via a PERK/eIF2α-dependent pathway. However, stearic acid-induced β-cell apoptosis was not obviously recovered. Conclusion: Our findings suggest the involvement of the lncRNA TCONS_00230836 in stearic acid-induced β-cell dysfunction, which provides novel insight into stearic acid-induced lipotoxicity to β cells. Anti-lncRNA TCONS_00230836 might be a new therapeutic strategy for alleviating stearic acid-induced β-cell dysfunction in the progression of T2DM.

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miR-29a-3p inhibits growth, proliferation, and invasion of papillary thyroid carcinoma by suppressing NF-κB signaling via direct targeting of OTUB2

Cited by 44 publications

References 35 publications

miR-326 inhibits the progression of papillary thyroid carcinoma by targeting MAPK1 and ERBB4

miR-326 inhibits the progression of papillary thyroid carcinoma by targeting MAPK1 and ERBB4

Aberrant expression profiles and bioinformatic analysis of CAF-derived exosomal miRNAs from three moderately differentiated supraglottic LSCC patients

TCONS_00230836 silencing restores stearic acid-induced β-cell dysfunction through alleviating endoplasmic reticulum stress via a PERK/eIF2α-dependent pathway rather than apoptosis

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