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10.3892/ol.2018.8341 http://scihub22266oqcxt.onion/10.3892/ol.2018.8341 C5962869!5962869!29849802     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncol+Lett 2018 ; 15 (5): 7963-72 Nephropedia Template TP {{tp|p=29849802|t=2018. HOTAIR contributes to the growth of liver cancer via targeting miR-217 |pdf=|usr=}}{{29849802}} gab.com Text HOTAIR contributes to the growth of liver cancer via targeting miR-217 JO: Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=29849802 #FOAvip Non-coding RNAs are important in the progression of liver cancer. The present study aimed to investigate the effects of long non-coding RNA HOX transcript antisense RNA (HOTAIR) on the proliferation of liver cancer and the association between HOTAIR and microRNA (miR)-217. It was demonstrated that the expression of HOTAIR was upregulated in liver cancer tissues and 3 liver cancer cell lines (MHCC97H, HepG2 and Hep3B). Inhibition of HOTAIR with HOTAIR small interfering (si) RNA lentiviral vectors significantly suppressed the cell proliferation of HepG2 cells, and downregulated the protein expression levels of two proliferation markers, Ki67 and proliferating cell nuclear antigen (PCNA). Furthermore, inhibition of HOTAIR induced G0/G1 cycle arrest by increasing the expression of p27 and decreasing the expression of cyclin D1. It was then predicted and verified that miR-217 was the target of HOTAIR. Expression of miR-217 was downregulated in liver cancer tissues and the 3 liver cancer cell lines. Further results revealed that inhibition of HOTAIR markedly upregulated the expression of miR-217 in HepG2 cells, and miR-217 inhibitor-induced reduction of miR-217 was significantly suppressed by HOTAIR inhibition. Furthermore, the increased cell proliferation and growth, the upregulated expression of Ki67 and PCNA, and the reduced G0/G1 cycle arrest induced by miR-217 inhibitor were partly rescued by inhibition of HOTAIR. Finally, the in vivo experiment indicated that HOTAIR inhibition suppressed tumorigenesis, including the smaller tumor volume and the reduced levels of Ki67. Overall, HOTAIR contributes to the proliferation and growth of liver cancer via downregulation of miR-217. Twit Text FOAVip HOTAIR contributes to the growth of liver cancer via targeting miR-217 ????Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=29849802 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29849802 #FOAvip English Wikipedia <ref>{{Cite pmid|29849802}}</ref> HOTAIR contributes to the growth of liver cancer via targeting miR-217 #MMPMID29849802 Wang LP; Wang JP; Wang XP Oncol Lett 2018[May]; 15 (5): 7963-72 PMID29849802show ga Non-coding RNAs are important in the progression of liver cancer. The present study aimed to investigate the effects of long non-coding RNA HOX transcript antisense RNA (HOTAIR) on the proliferation of liver cancer and the association between HOTAIR and microRNA (miR)-217. It was demonstrated that the expression of HOTAIR was upregulated in liver cancer tissues and 3 liver cancer cell lines (MHCC97H, HepG2 and Hep3B). Inhibition of HOTAIR with HOTAIR small interfering (si) RNA lentiviral vectors significantly suppressed the cell proliferation of HepG2 cells, and downregulated the protein expression levels of two proliferation markers, Ki67 and proliferating cell nuclear antigen (PCNA). Furthermore, inhibition of HOTAIR induced G0/G1 cycle arrest by increasing the expression of p27 and decreasing the expression of cyclin D1. It was then predicted and verified that miR-217 was the target of HOTAIR. Expression of miR-217 was downregulated in liver cancer tissues and the 3 liver cancer cell lines. Further results revealed that inhibition of HOTAIR markedly upregulated the expression of miR-217 in HepG2 cells, and miR-217 inhibitor-induced reduction of miR-217 was significantly suppressed by HOTAIR inhibition. Furthermore, the increased cell proliferation and growth, the upregulated expression of Ki67 and PCNA, and the reduced G0/G1 cycle arrest induced by miR-217 inhibitor were partly rescued by inhibition of HOTAIR. Finally, the in vivo experiment indicated that HOTAIR inhibition suppressed tumorigenesis, including the smaller tumor volume and the reduced levels of Ki67. Overall, HOTAIR contributes to the proliferation and growth of liver cancer via downregulation of miR-217. äHOTAIR contributes to the growth of liver cancer via targeting miR-217(epmc).pdf DeepDyve Pubget Overpricing