miR‐4299 mediates the invasive properties and tumorigenicity of human follicular thyroid carcinoma by targeting <scp>ST</scp>6<scp>GALNAC</scp>4

Miao, Xudong; Li, Jia; Zhou, Huimin; Song, Xianmin; Zhou, Ming; Xu, Jinchao; Zhao, Lifen; Feng, Xueping; Zhao, Yongfu

doi:10.1002/iub.1467

Cited by 24 publications

(21 citation statements)

References 29 publications

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“…ST6GALNAC2 regulates breast cancer invasion 40 , 41 . In FTC research, we found that ST6GALNAC4 and ST6GALNAC2 modulate tumourigenicity of FTC 17 , 42 and that miR146a/b promotes FTC cell proliferation via the inhibition of ST8SIA4 16 . In the current study, ST6GAL2 was more highly expressed in FTC tissues and cell lines compared with normal tissues and cell lines.…”

Section: Discussionmentioning

confidence: 96%

“…In previous studies, protein synthesis was shown to be modulated by miRNAs that are able to bind to the 3′-untranslated region of target mRNAs 15 . According to our previous research, miR146a/b promotes FTC cell proliferation via the inhibition of ST8SIA4; 16 moreover, miR-4299 regulates FTC cell invasiveness by targeting ST6GALNAC4 17 . In addition, increasing experimental evidence suggests that lncRNAs functionally target miRNAs, which can be sponged by lncRNAs.…”

Section: Introductionmentioning

confidence: 87%

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LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge

et al. 2018

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Long non-coding RNAs (lncRNAs), which are important functional regulators in cancer, have received increased attention in recent years. In this study, next-generation sequencing technology was used to identify aberrantly expressed lncRNAs in follicular thyroid carcinoma (FTC). The long non-coding RNA–HLA complex P5 (HCP5) was found to be overexpressed in FTC. The results of the qPCR analysis were consistent with the sequencing results. In addition, functional experiments showed that overexpression of HCP5 can promote the proliferation, migration, invasiveness and angiogenic ability of FTC cells. Furthermore, according to the sequencing results, HCP5 and alpha-2, 6-sialyltransferase 2 (ST6GAL2) were co-expressed in FTC. We hypothesised that ST6GAL2 may be regulated by HCP5, which would in turn mediate the activity of FTC cells. Through qPCR, immunostaining analyses and functional experiments, we determined that the expression of HCP5 was elevated and was correlated with the levels of ST6GAL2 in FTC tissues and cells. Mechanistic experiments showed that HCP5 functions as a competing endogenous RNA (ceRNA) and acts as a sponge for miR-22-3p, miR-186-5p and miR-216a-5p, which activates ST6GAL2. In summary, our study revealed that HCP5 is a tumour regulator in the development of FTC and that it may contribute to improvement of FTC diagnosis and therapy.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 87%

LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge

et al. 2018

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“…Research on this remains limited, but some recent studies investigated functional relationship of sialic acid phenotypes and malignant character of thyroid cancers. The suppression of the ST6GalNAc IV enzyme using miRNAs in follicular carcinoma cell lines significantly reduced their invasive and malignant characters . In addition, it has been reported that blocking the activity of the phosphotidylinositol 3‐kinase (PI3K)/Akt signaling with specific inhibitors results in the inactivation of the ST6GalNAc II enzyme, thereby reducing the invasive character of follicular cancer cells .…”

Section: Discussionmentioning

confidence: 99%

“…The suppression of the ST6GalNAc IV enzyme using miRNAs in follicular carcinoma cell lines significantly reduced their invasive and malignant characters. 16 In addition, it has been reported that blocking the activity of the phosphotidylinositol 3-kinase (PI3K)/Akt signaling with specific inhibitors results in the inactivation of the ST6Gal-NAc II enzyme, thereby reducing the invasive character of follicular cancer cells. 17 The residues of α1,6 fucose are found in the initial GlcNAc molecule of N-linked oligosaccharides and transferred to this molecule by the enzyme FUT8.…”

Section: Discussionmentioning

confidence: 99%

The effect of plant lectins on the survival and malignant behaviors of thyroid cancer cells

Kaptan

Sancar-Bas

Sancakli

et al. 2018

J of Cellular Biochemistry

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Altered or aberrant glycosylation is a common phenomenon in cancer cells and it originates from changes in the expression of the enzymes, glycosyltransferase, and glycosidase which up-regulate in response to some oncogenes in the glycan synthesis pathway. In this present study, it has been aimed to determine the alteration of sialic acid and fucose expressions in the cell surface of human thyroid carcinoma cells and investigate the changes in tumorigenic and malignant characters after treating them with specific plant lectins. Our study showed that the cell surface glycan chains of anaplastic 8305C, follicular FTC-133, and papillary K1 thyroid carcinoma cells were rich in α-2,6, α-2,3, sialic acid, and α-1,6 fucose residues. When the cells were treated with specific doses of Maackia amurensis lectin II (MAL), Sambucus nigra agglutinin (SNA), and Aleuria aurantia lectin (AAL) which have specific binding capacity for the detected glycan residues, respectively their cancerous traits changed dramatically. Remarkable findings obtained from MAL treatment leading to necrosis in 8505C cells without any toxicity for normal thyroid epithelial cells but it had proliferative effect on K1 and FCT-133 cells. Besides, MAL and SNA treatment decreased the mobility of 8505C and K1 cells. MAL and SNA lectins dramatically reduced the endothelial affinity of the cells and AAL significantly attenuated that of 8050C and K1 cells but not FTC-133. These results suggest that altered cell surface glycosylation in thyroid cancer seems to be a strong candidate for developing new therapeutic strategies.

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“…It has been reported that miR-4701-5p is responsible for multi drug resistance of chronic myeloid leukemia cells, at least in part, by targeting and down-regulating ST3GAL1 [103]. The invasive properties and tumorigenicity of human follicular thyroid carcinoma is mediated by miR-4299, through targeting and silencing ST6GALNAC4 [104]. …”

Section: Epigenetic-regulation Of Cancer Associated Structuresmentioning

confidence: 99%

Epigenetic Bases of Aberrant Glycosylation in Cancer

Dall’Olio

Trinchera

2017

IJMS

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In this review, the sugar portions of glycoproteins, glycolipids, and glycosaminoglycans constitute the glycome, and the genes involved in their biosynthesis, degradation, transport and recognition are referred to as “glycogenes“. The extreme complexity of the glycome requires the regulatory layer to be provided by the epigenetic mechanisms. Almost all types of cancers present glycosylation aberrations, giving rise to phenotypic changes and to the expression of tumor markers. In this review, we discuss how cancer-associated alterations of promoter methylation, histone methylation/acetylation, and miRNAs determine glycomic changes associated with the malignant phenotype. Usually, increased promoter methylation and miRNA expression induce glycogene silencing. However, treatment with demethylating agents sometimes results in silencing, rather than in a reactivation of glycogenes, suggesting the involvement of distant methylation-dependent regulatory elements. From a therapeutic perspective aimed at the normalization of the malignant glycome, it appears that miRNA targeting of cancer-deranged glycogenes can be a more specific and promising approach than the use of drugs, which broad target methylation/acetylation. A very specific type of glycosylation, the addition of GlcNAc to serine or threonine (O-GlcNAc), is not only regulated by epigenetic mechanisms, but is an epigenetic modifier of histones and transcription factors. Thus, glycosylation is both under the control of epigenetic mechanisms and is an integral part of the epigenetic code.

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miR‐4299 mediates the invasive properties and tumorigenicity of human follicular thyroid carcinoma by targeting ST6GALNAC4

Cited by 24 publications

References 29 publications

LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge

LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge

The effect of plant lectins on the survival and malignant behaviors of thyroid cancer cells

Epigenetic Bases of Aberrant Glycosylation in Cancer

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