Heparan sulfate D-glucosamine 3-O-sulfotransferase 3B1 is a novel regulator of transforming growth factor-beta-mediated epithelial-to-mesenchymal transition and regulated by miR-218 in nonsmall cell lung cancer
0301 basic medicine
Epithelial-Mesenchymal Transition
Lung Neoplasms
3. Good health
Gene Expression Regulation, Neoplastic
MicroRNAs
03 medical and health sciences
Phenotype
Genes, Reporter
Transforming Growth Factor beta
Carcinoma, Non-Small-Cell Lung
Cell Line, Tumor
Gene Knockdown Techniques
Humans
RNA Interference
Sulfotransferases
DOI:
10.4103/jcrt.jcrt_659_17
Publication Date:
2018-03-07T05:50:57Z
AUTHORS (4)
ABSTRACT
Due to high metastasis and recurrence rate. Recent studies indicated that epithelial-to-mesenchymal transition (EMT) was involved in the progression and metastasis in cancer. Some reports also indicate that HS3ST3B1 played a role in angiogenesis and the proliferation of cancer cells. In this study, we aim to investigate its role in non-small cell lung cancer (NSCLC) .All cell lines were purchased from ATCC and cultured in our central lab. RT-PCR was performed to study the expession of HS3ST3B1 in tumors and matched normal tissues. Western-blot was used to investigate the expession of HS3ST3B1 in cell lines. We also used luciferase report system to confirm the regulation of HS3ST3B1 by miR-218 in cells.In this study, we found that HS3ST3B1 was significantly upregulated in NSCLC tissues compared with matched normal tissues (P = 0.02). Its expression was also up-regulated in mesenchymal phenotype of NSCLC cell lines compared with epithelial phenotype (P < 0.05). When TGF-β was applied to induce the epithelial phenotype to mesenchymal phenotype, it was upregulated compared with previous epithelial cell lines. When HS3ST3B1 was knocked down by specific small interfering RNA in the mesenchymal phenotype, mesenchymal phenotype was transformed to epithelial phenotype. Moreover, we also found that it could be targeted by miR-218 in NSCLC.These findings indicate that HS3ST3B1 is a novel regulator of TGF-beta-mediated EMT and is regulated by miR-218 in NSCLC.
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