Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1166/jnn.2019.16404 http://scihub22266oqcxt.onion/10.1166/jnn.2019.16404 30486934!ä!30486934 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 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       J+Nanosci+Nanotechnol 2019 ; 19 (4): 1942-1950 Nephropedia Template TP {{tp|p=30486934|t=2019. Ginsenoside Rh2 Inhibits Angiogenesis in Prostate Cancer by Targeting CNNM1 |pdf=|usr=}}{{30486934}} gab.com Text Ginsenoside Rh2 Inhibits Angiogenesis in Prostate Cancer by Targeting CNNM1 JO: J Nanosci Nanotechnol http://www.kidney.de/pget.php?&tw=1&pmid=30486934 #FOAvip To explore the molecular mechanism by which ginsenoside Rh2 (G-Rh2) inhibits prostate cancer by regulating vascular growth. Different concentrations of G-Rh2 with three prostate cancer cell lines (LNCaP, PC3 and DU145) were transplanted in nude mice, and tumor mass volume was measured over time. LNCaP, PC3 and DU145 were co-cultured with vascular endothelial cells to determine the optimal concentration of G-Rh2 by MTT assay. LNCaP, PC3 and DU145 were cultured under the selected concentration (0, 0.01, 0.05, 0.1, 0.5 and 1 mg/mL) of G-Rh2, and the expression levels of CD31, VEGF, PDGF and CNNM1 detected by qRT-PCR and western blot. The expression pattern of CD31 was detected in CNNM1 overexpressed and knockout LNCaP, PC3 and DU145 cells under G-Rh2. G-Rh2 significantly inhibited the growth of all three prostate cancer cell lines in the dorsum of nude mice (P <0.05), and the increment rate of vascular endothelial cells co-cultured with LNCaP, PC3 and DU145 (P <0.05). The expression of CD31, VEGF, PDGF and CNNM1 genes in LNCaP, PC3 and DU145 cells was inhibited by G-Rh2. Overexpression of CNNM1 reversed the inhibitory effect of G-Rh2 on the expression of CD31 in these cells (P <0.05), while the function of knockout of CNNM1 and the inhibitory effect of G-Rh2 appeared to be similar (P <0.05). In conclusion, G-Rh2 inhibited prostate cancer growth by inhibiting its angiogenesis through decreasing the expression of CNNM1 in the cancer cells. Twit Text FOAVip Ginsenoside Rh2 Inhibits Angiogenesis in Prostate Cancer by Targeting CNNM1 ????J Nanosci Nanotechnol http://www.kidney.de/pget.php?&tw=1&pmid=30486934 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30486934 #FOAvip English Wikipedia <ref>{{Cite pmid|30486934}}</ref> Ginsenoside Rh2 Inhibits Angiogenesis in Prostate Cancer by Targeting CNNM1 #MMPMID30486934 Huang Y; Huang H; Han Z; Li W; Mai Z; Yuan R J Nanosci Nanotechnol 2019[Apr]; 19 (4): 1942-1950 PMID30486934show ga To explore the molecular mechanism by which ginsenoside Rh2 (G-Rh2) inhibits prostate cancer by regulating vascular growth. Different concentrations of G-Rh2 with three prostate cancer cell lines (LNCaP, PC3 and DU145) were transplanted in nude mice, and tumor mass volume was measured over time. LNCaP, PC3 and DU145 were co-cultured with vascular endothelial cells to determine the optimal concentration of G-Rh2 by MTT assay. LNCaP, PC3 and DU145 were cultured under the selected concentration (0, 0.01, 0.05, 0.1, 0.5 and 1 mg/mL) of G-Rh2, and the expression levels of CD31, VEGF, PDGF and CNNM1 detected by qRT-PCR and western blot. The expression pattern of CD31 was detected in CNNM1 overexpressed and knockout LNCaP, PC3 and DU145 cells under G-Rh2. G-Rh2 significantly inhibited the growth of all three prostate cancer cell lines in the dorsum of nude mice (P <0.05), and the increment rate of vascular endothelial cells co-cultured with LNCaP, PC3 and DU145 (P <0.05). The expression of CD31, VEGF, PDGF and CNNM1 genes in LNCaP, PC3 and DU145 cells was inhibited by G-Rh2. Overexpression of CNNM1 reversed the inhibitory effect of G-Rh2 on the expression of CD31 in these cells (P <0.05), while the function of knockout of CNNM1 and the inhibitory effect of G-Rh2 appeared to be similar (P <0.05). In conclusion, G-Rh2 inhibited prostate cancer growth by inhibiting its angiogenesis through decreasing the expression of CNNM1 in the cancer cells. |*Endothelial Cells[MESH] |*Prostatic Neoplasms/drug therapy/genetics[MESH] |Animals[MESH] |Cell Line, Tumor[MESH] |Ginsenosides[MESH] |Humans[MESH] |Male[MESH] |Mice[MESH]Ginsenoside Rh2 Inhibits Angiogenesis in Prostate Cancer by Targeting (epmc).pdf DeepDyve Pubget Overpricing