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10.7150/jca.17958 http://scihub22266oqcxt.onion/10.7150/jca.17958 C5381176!5381176!28382150     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cancer 2017 ; 8 (5): 870-9 Nephropedia Template TP {{tp|p=28382150|t=2017. MiR-93 Promotes Tumorigenesis and Metastasis of Non-Small Cell Lung Cancer Cells by Activating the PI3K/Akt Pathway via Inhibition of LKB1/PTEN/CDKN1A |pdf=|usr=}}{{28382150}} gab.com Text MiR-93 Promotes Tumorigenesis and Metastasis of Non-Small Cell Lung Cancer Cells by Activating the PI3K/Akt Pathway via Inhibition of LKB1/PTEN/CDKN1A JO: J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28382150 #FOAvip Background: Non-small cell lung cancer (NSCLC) accounts for approximately 85% of clinical lung cancer cases. MicroRNA-93 (miR-93) is an oncomiR in many types of human cancer, exerting pivotal effects in the development and progression of malignancies, including NSCLC. However, the mechanism underlying miR-93 involvement in NSCLC is unknown. Our purpose was to reveal and explain this mechanism, with the goal of contributing to the development of new diagnostic biomarkers and individualized therapeutic tools.Methods: The expression of miR-93 was determined in NSCLC cell lines A549, H1975, and H1299. The cells were transfected with control plasmids (Mock group), miR-93 overexpression plasmids (miR-93 Up group), or miR-93 inhibitor plasmids (miR-93 Down group) to generate stable miR-93-overexpressing or -depleted cells. The effects of miR-93 on proliferation, migration, and invasion of these cells were determined. The in vivo effects of miR-93 on tumor metastasis were determined in an NSCLC xenograft mouse model. The molecular mechanisms underlying these effects were investigated via dual luciferase reporter assay and western blotting.Results: MiR-93 expression levels were significantly greater in the NSCLC cell lines than in normal lung epithelial cells. Cell proliferation, migration, and invasion were significantly stimulated by miR-93 upregulation (all P<0.05) and inhibited by miR-93 downregulation. Dual luciferase reporter assay demonstrated that miR-93 directly bound with the 3?-untranslated region of the tumor suppressor gene LKB1. Western blotting analysis indicated that miR-93 activated the PI3K/Akt pathway by inhibiting LKB1, PTEN, and p21. Increased expression of miR-93 induced significant hepatic metastasis of lung cancer in the xenograft mouse model.Conclusion: Overexpression of miR-93 facilitates tumorigenesis and metastasis of NSCLC. These findings provide novel insight into the mechanism of miR-93 involvement in NSCLC, suggesting that miR-93 may serve as a potential therapeutic target. Twit Text FOAVip MiR-93 Promotes Tumorigenesis and Metastasis of Non-Small Cell Lung Cancer Cells by Activating the PI3K/Akt Pathway via Inhibition of LKB1/PTEN/CDKN1A ????J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28382150 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28382150 #FOAvip English Wikipedia <ref>{{Cite pmid|28382150}}</ref> MiR-93 Promotes Tumorigenesis and Metastasis of Non-Small Cell Lung Cancer Cells by Activating the PI3K/Akt Pathway via Inhibition of LKB1/PTEN/CDKN1A #MMPMID28382150 Li C; Lyu J; Meng QH J Cancer 2017[]; 8 (5): 870-9 PMID28382150show ga Background: Non-small cell lung cancer (NSCLC) accounts for approximately 85% of clinical lung cancer cases. MicroRNA-93 (miR-93) is an oncomiR in many types of human cancer, exerting pivotal effects in the development and progression of malignancies, including NSCLC. However, the mechanism underlying miR-93 involvement in NSCLC is unknown. Our purpose was to reveal and explain this mechanism, with the goal of contributing to the development of new diagnostic biomarkers and individualized therapeutic tools.Methods: The expression of miR-93 was determined in NSCLC cell lines A549, H1975, and H1299. The cells were transfected with control plasmids (Mock group), miR-93 overexpression plasmids (miR-93 Up group), or miR-93 inhibitor plasmids (miR-93 Down group) to generate stable miR-93-overexpressing or -depleted cells. The effects of miR-93 on proliferation, migration, and invasion of these cells were determined. The in vivo effects of miR-93 on tumor metastasis were determined in an NSCLC xenograft mouse model. The molecular mechanisms underlying these effects were investigated via dual luciferase reporter assay and western blotting.Results: MiR-93 expression levels were significantly greater in the NSCLC cell lines than in normal lung epithelial cells. Cell proliferation, migration, and invasion were significantly stimulated by miR-93 upregulation (all P<0.05) and inhibited by miR-93 downregulation. Dual luciferase reporter assay demonstrated that miR-93 directly bound with the 3?-untranslated region of the tumor suppressor gene LKB1. Western blotting analysis indicated that miR-93 activated the PI3K/Akt pathway by inhibiting LKB1, PTEN, and p21. Increased expression of miR-93 induced significant hepatic metastasis of lung cancer in the xenograft mouse model.Conclusion: Overexpression of miR-93 facilitates tumorigenesis and metastasis of NSCLC. These findings provide novel insight into the mechanism of miR-93 involvement in NSCLC, suggesting that miR-93 may serve as a potential therapeutic target. äMiR-93 Promotes Tumorigenesis and Metastasis of Non-Small Cell Lung Ca(epmc).pdf DeepDyve Pubget Overpricing