ST6GalNAcII mediates tumor invasion through PI3K/Akt/NF-κB signaling pathway in follicular thyroid carcinoma

Miao, Xudong; Zhao, Yongfu

doi:10.3892/or.2016.4590

Cited by 18 publications

(18 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, little is known regarding the relationship between ST6GALNAC2 and chemoresistance in CRC. ST6GALNAC2 was identified down‐regulated in follicular thyroid carcinoma and breast cancer, and the differential expression was in accordance with our current results. ST6GALNAC2 expressed a lower level in CRC tissues and 5‐FU‐resistant CRC cell lines.…”

Section: Discussionsupporting

confidence: 91%

“…Over‐expressed molecules of PI3K/AKT pathway, caused by aberrant sialylation, resulted in the evolution of AML . ST6GALNAC2 played a crucial role in the procession of follicular thyroid carcinoma and breast cancer via PI3K/AKT pathway. Surprisingly, sufficient evidence has been provided that miRNAs could modulate the activity of PI3K/AKT pathways .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Upregulation of microRNA‐135b and microRNA‐182 promotes chemoresistance of colorectal cancer by targeting ST6GALNAC2 via PI3K/AKT pathway

Liu

Zhao

et al. 2017

Molecular Carcinogenesis

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are increasingly involved in the development of drug resistance, including 5-fluorouracil (5-FU) resistance in colorectal cancer (CRC). Aberrant sialylation is correlated with human CRC. The study was to explore whether miR-135b and miR-182 modulated 5-FU chemoresistance of CRC by targeting ST6GALNAC2 via PI3K/AKT pathway. MiR-135b and miR-182 were found to be up-regulated in CRC tissues and 5-FU resistant CRC cell lines. Forced miR-135b and miR-182 expression also affected ST6GALNAC2 levels. Using reporter-gene assay, ST6GALNAC2 was identified as direct target of miR-135b and miR-182, while ST6GALNAC2 expression exhibited patterns opposite to that of miR-135b and miR-182 in CRC samples and cell lines. Interestingly, up-regulation of miR-135b or miR-182 increased drug resistance and proliferation, but decreased apoptosis in 5-FU resistant CRC cell lines. Suppression of these miRNAs implicated an inverse function, while altered expression of ST6GALNAC2 mediated CRC progression upon transfection with miR-135b/-182 mimic or inhibitor. Furthermore, miR-135b and miR-182 were clarified to regulate the activity of phosphoinositide-3 kinase (PI3K)/AKT pathway. Inhibition of the PI3K/AKT pathway enhanced the chemosensitivity to 5-FU in HCT-8/5-FU and LoVo/5-FU. Taken together, miR-135b and miR-182 may reverse the resistance to 5-FU in CRC cells by targeting ST6GALNAC2 via PI3K/AKT pathway, which render potential chemotherapy targets for the treatment of CRC.

show abstract

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Upregulation of microRNA‐135b and microRNA‐182 promotes chemoresistance of colorectal cancer by targeting ST6GALNAC2 via PI3K/AKT pathway

Liu

Zhao

et al. 2017

Molecular Carcinogenesis

View full text Add to dashboard Cite

show abstract

“…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%

LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge

et al. 2018

Self Cite

View full text Add to dashboard Cite

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.

show abstract

“…A xenograft of FTC-238 cells with silenced ST6GalNAc2 showed lower tumor volume in mice, as compared with the control FTC-238 xenograft. Overexpression of ST6GalNAc2 in the FTC-133 non-invasive cell line enhanced its invasive ability and increased the tumor volume in xenograft mouse [ 104 ].…”

Section: Glycosylation In Thyroid Pathologymentioning

confidence: 99%

Glycosylation in the Thyroid Gland: Vital Aspects of Glycoprotein Function in Thyrocyte Physiology and Thyroid Disorders

Ząbczyńska

Kozłowska

Pocheć

2018

IJMS

View full text Add to dashboard Cite

The key proteins responsible for hormone synthesis in the thyroid are glycosylated. Oligosaccharides strongly affect the function of glycosylated proteins. Both thyroid-stimulating hormone (TSH) secreted by the pituitary gland and TSH receptors on the surface of thyrocytes contain N-glycans, which are crucial to their proper activity. Thyroglobulin (Tg), the protein backbone for synthesis of thyroid hormones, is a heavily N-glycosylated protein, containing 20 putative N-glycosylated sites. N-oligosaccharides play a role in Tg transport into the follicular lumen, where thyroid hormones are produced, and into thyrocytes, where hyposialylated Tg is degraded. N-glycans of the cell membrane transporters sodium/iodide symporter and pendrin are necessary for iodide transport. Some changes in glycosylation result in abnormal activity of the thyroid and alteration of the metabolic clearance rate of hormones. Alteration of glycan structures is a pathological process related to the progression of chronic diseases such as thyroid cancers and autoimmunity. Thyroid carcinogenesis is accompanied by changes in sialylation and fucosylation, β1,6-branching of glycans, the content and structure of poly-LacNAc chains, as well as O-GlcNAcylation, while in thyroid autoimmunity the main processes affected are sialylation and fucosylation. The glycobiology of the thyroid gland is an intensively studied field of research, providing new data helpful in understanding the role of the sugar component in thyroid protein biology and disorders.

show abstract

ST6GalNAcII mediates tumor invasion through PI3K/Akt/NF-κB signaling pathway in follicular thyroid carcinoma

Cited by 18 publications

References 29 publications

Upregulation of microRNA‐135b and microRNA‐182 promotes chemoresistance of colorectal cancer by targeting ST6GALNAC2 via PI3K/AKT pathway

Upregulation of microRNA‐135b and microRNA‐182 promotes chemoresistance of colorectal cancer by targeting ST6GALNAC2 via PI3K/AKT pathway

LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge

Glycosylation in the Thyroid Gland: Vital Aspects of Glycoprotein Function in Thyrocyte Physiology and Thyroid Disorders

Contact Info

Product

Resources

About