The Effect of miR-98 and miR-214 on Apoptotic and Angiogenic Pathways in Hepatocellular Carcinoma HepG2 Cells
Hepatocellular carcinoma (HCC) is one of the foremost causes of cancer related morbidity worldwide. An increasing number of studies have confirmed that microRNAs play an important role in the development, progression and metastasis of HCC. From those important miRNAs are miR-98 and miR-214. This stu...
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Published in: | Indian journal of clinical biochemistry Vol. 35; no. 3; pp. 353 - 358 |
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Main Authors: | , |
Format: | Journal Article |
Language: | English |
Published: |
New Delhi
Springer India
01-07-2020
Springer Springer Nature B.V |
Subjects: | |
Online Access: | Get full text |
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Summary: | Hepatocellular carcinoma (HCC) is one of the foremost causes of cancer related morbidity worldwide. An increasing number of studies have confirmed that microRNAs play an important role in the development, progression and metastasis of HCC. From those important miRNAs are miR-98 and miR-214. This study were conducted to explore the effect of these two miRNAs on some apoptotic and angiogenic genes namely, BCL-2, survivin, CCND1, CDC2, P53 and P21, VEGF, Hif-1α, MMP-2, MMP-9, Ang-1, Ang-2, and FGF-1. miRNAs mimics and inhibitors transfection was used to investigate the role of both studied molecules in apoptosis and angiogenesis in HepG2 cells. QRT-PCR was used for Quantitative gene and miRNA expression analyses. The study revealed that miR-98 could serve as a pro-apoptotic factor through the upregulation of P53 gene expression levels. Besides, the anti-angiogenic effect of this miRNA was evident through the down regulation of Ang-1 and FGF-1 genes. Meanwhile, miR-214 showed a pro-apoptotic role and anti-angiogenic effects. These effects were verified through the significant down regulation of BCL-2, CDC2, VEGF, Ang-1 and MMP-2. These results introduced a possible positive role played by both miR-98 and miR-214 on some pro-apoptotic and anti-angiogenic genes. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0970-1915 0974-0422 |
DOI: | 10.1007/s12291-019-00824-1 |