Knockdown of long non-coding RNA PVT1 suppresses cell proliferation and invasion of colorectal cancer via upregulation of microRNA-214-3p.

This study aimed to investigate the regulatory role of lncRNA PVT1 in CRC. Subcellular localization detected by fluorescence in situ hybridization identified that lncRNA PVT1 was primarily located in the cytoplasm. The interaction between lncRNA PVT1 and microRNA-214-3p (miR-214-3p) and IRS1 was predicted using RNA22 website. Next, the dual luciferase reporter gene assay, RNA pull-down and RIP assays verified lncRNA PVT1 to be a competitive endogenous RNA (ceRNA) against miR-214-3p, and IRS1 was found to be a target of miR-214-3p. The expression pattern of lncRNA PVT1, miR-214-3p, IRS1, PI3K and Akt was characterized in response to lncRNA PVT1 silencing or miR-214-3p up-regulation. Meanwhile, their regulatory effects on cell proliferation, invasion and apoptosis were detected in CRC cells. With increased levels of miR-214-3p and decreased levels of lncRNA PVT1 in CRC cells, the expression of PI3K and Akt was reduced, and consequently, the cell apoptosis was stimulated and cell proliferation and invasion were suppressed. All in all, lncRNA PVT1 competitively binds to miR-214-3p to up-regulate the expression of IRS1 through activation of the PI3K/Akt signaling pathway, thus accelerating CRC progression. This study suggests that lncRNA PVT1 might be a potential target of therapeutic strategies for CRC treatment. PMID: 31125260 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Gastrointestinal and Liver Physiology - Category: Physiology Authors: Tags: Am J Physiol Gastrointest Liver Physiol Source Type: research

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Publication date: Available online 9 December 2019Source: European UrologyAuthor(s): Christian Radmayr
Source: European Urology - Category: Urology & Nephrology Source Type: research
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Source: Artificial Cells, Nanomedicine and Biotechnology - Category: Biotechnology Tags: Artif Cells Nanomed Biotechnol Source Type: research
CONCLUSIONS Our results suggest that PVT1 could promote metastasis and proliferation of colon cancer via endogenous sponging and inhibiting the expression of miR-26b, which may highlight the significance of lncRNA PVT1 in colon cancer tumorigenesis. PMID: 30504754 [PubMed - in process]
Source: Medical Science Monitor - Category: Research Tags: Med Sci Monit Source Type: research
Knockdown of long non‑coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. Mol Med Rep. 2018 Apr 20;: Authors: Fan H, Zhu JH, Yao XQ Abstract Multidrug resistance (MDR) is one of the primary causes of chemotherapy failure in colorectal cancer (CRC), and extensive biological studies into MDR are required. The non‑coding RNA plasmacytoma variant translocation 1 (PVT1) has been demonstrated to be associated with low survival rates in patients with CRC. However, whether PVT1 serves a critical function in the MDR of CRC remains to be determined. To determine the association between ...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research
Authors: Wang C, Zhu X, Pu C, Song X Abstract Emerging evidence indicates that the long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) is associated with tumourigenesis in various types of cancer. However, its specific effects on the proliferation, invasion and metastasis of colorectal cancer (CRC) are still poorly understood. The present study aimed to investigate PVT1 expression in CRC and explore its role in CRC pathogenesis. The reverse transcriptase‑quantitative polymerase chain reaction (RT‑qPCR) technique was used to assess PVT1 expression in CRC cell lines. Gene Expression Omni...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research
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Source: American Journal of Translational Research - Category: Research Tags: Am J Transl Res Source Type: research
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Source: Cell Proliferation - Category: Cytology Authors: Tags: REVIEW ARTICLE Source Type: research
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Source: Cancer Medicine - Category: Cancer & Oncology Authors: Tags: Original Research Source Type: research
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