Objective: To investigate the influences of long non-coding ribonucleic acid (lncRNA) H19 on proliferation and apoptosis of nephroblastoma cells.
Materials And Methods: A total of 5 pairs of nephroblastoma tissues and paraneoplastic tissues were obtained. Gene expression levels of lncRNA H19, microRNA (miR)-675, and transforming growth factor beta induced (TGFBI) were detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Their regulatory effects on the viability of nephroblastoma cells were examined by Cell Counting Kit-8 (CCK-8) assay. Finally, the apoptosis level in each group was detected through TUNEL assay, and the protein expressions of TGFBI and Caspase-8 were examined using Western blotting (WB) assay.
Results: The gene expression levels of lncRNA H19 and miR-675 were markedly downregulated in nephroblastoma tissues (p<0.05), while that of TGFBI was notably upregulated (p<0.05). LncRNA H19 could reduce the proliferative ability of HFWT cells (p<0.05) and stimulates apoptosis rate (p<0.05). It upregulated the expressions of miR-675 and Caspase-8 (p<0.05), and downregulated TGFBI (p<0.05). Besides, miR-675 was able to upregulate Caspase-8 (p<0.05) and downregulate TGFBI (p<0.05). In addition, the protein expression of Caspase-8 was downregulated (p<0.05), while that of TGFBI was upregulated (p<0.05) after the knockdown of miR-675 in HFWT cells.
Conclusions: LncRNA H19 may inhibit TGFBI expression by regulating miR-675 level, so as to weaken the proliferation and enhance the apoptosis of nephroblastoma cells.
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http://dx.doi.org/10.26355/eurrev_202206_28947 | DOI Listing |
Comput Biol Chem
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Institute of Global Health and Human Ecology (IGHHE), School of Sciences and Engineering, The American University in Cairo, New Cairo 11835, Egypt. Electronic address:
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J Cancer
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Amity Institute of Molecular Medicine and Stem Cell Research (AIMMSCR), Amity University, Sector-125, Noida 201313, Uttar Pradesh, India. Electronic address:
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and grave malignancies with confined and ineffective therapeutic options. XPO1 is a critical regulator of nuclear export and activation of tumor suppressor proteins. The present study evaluated the therapeutic potential and molecular mechanisms of XPO1 inhibition against PDAC.
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