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10.1016/j.cbi.2019.01.036 http://scihub22266oqcxt.onion/10.1016/j.cbi.2019.01.036 30710498!ä!30710498 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Chem+Biol+Interact 2019 ; 302 (ä): 83-92 Nephropedia Template TP {{tp|p=30710498|t=2019. miR-543 inhibites cervical cancer growth and metastasis by targeting TRPM7 |pdf=|usr=}}{{30710498}} gab.com Text miR-543 inhibites cervical cancer growth and metastasis by targeting TRPM7 JO: Chem Biol Interact http://www.kidney.de/pget.php?&tw=1&pmid=30710498 #FOAvip Dysregulation of miR-543 has been implicated to play crucial roles in various human cancers. However, the function of miR-543 involved in cervical cancer (CC) progress remains largely unknown. Thus, this study aimed to explore the potential role of miR-543 and the underlying mechanisms in human CC. In this study, we found that miR-543 was significantly downregulated in 69 CC tissue samples and cell lines when compared to adjacent normal tissues and cell line. Decreased miR-543 was closely correlated with poor clinicopathological parameters including larger tumor size, late FIGO stage and lymph node metastasis. Overexpression of miR-543 in CC cell lines remarkably inhibited cell proliferation, invasion and migration, caused cell cycle arrest, promoted apoptosis in vitro, and suppressed tumor growth in vivo, whereas miR-543 inhibitor showed the opposite effect. Dual-luciferase assay validated that 3'-untranslated region (UTR) of transient receptor potential melastatin 7 (TRPM7) was a direct binding site of miR-543. Rescue experiments showed that restoration of TRPM7 expression partially reversed the miR-543-mediated inhibition of proliferation and invasion in CC cells. Further studies confirmed that P13K/AKT and p38/MAPK signaling was involved in miR-543/TRPM7 axis mediated CC progression. Thus, these findings demonstrated the tumor suppressor role of miR-543 on CC progression, which might serve as a potential biomarker for CC diagnosis and therapy. Twit Text FOAVip miR-543 inhibites cervical cancer growth and metastasis by targeting TRPM7 ????Chem Biol Interact http://www.kidney.de/pget.php?&tw=1&pmid=30710498 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30710498 #FOAvip English Wikipedia <ref>{{Cite pmid|30710498}}</ref> miR-543 inhibites cervical cancer growth and metastasis by targeting TRPM7 #MMPMID30710498 Liu X; Gan L; Zhang J Chem Biol Interact 2019[Apr]; 302 (ä): 83-92 PMID30710498show ga Dysregulation of miR-543 has been implicated to play crucial roles in various human cancers. However, the function of miR-543 involved in cervical cancer (CC) progress remains largely unknown. Thus, this study aimed to explore the potential role of miR-543 and the underlying mechanisms in human CC. In this study, we found that miR-543 was significantly downregulated in 69 CC tissue samples and cell lines when compared to adjacent normal tissues and cell line. Decreased miR-543 was closely correlated with poor clinicopathological parameters including larger tumor size, late FIGO stage and lymph node metastasis. Overexpression of miR-543 in CC cell lines remarkably inhibited cell proliferation, invasion and migration, caused cell cycle arrest, promoted apoptosis in vitro, and suppressed tumor growth in vivo, whereas miR-543 inhibitor showed the opposite effect. Dual-luciferase assay validated that 3'-untranslated region (UTR) of transient receptor potential melastatin 7 (TRPM7) was a direct binding site of miR-543. Rescue experiments showed that restoration of TRPM7 expression partially reversed the miR-543-mediated inhibition of proliferation and invasion in CC cells. Further studies confirmed that P13K/AKT and p38/MAPK signaling was involved in miR-543/TRPM7 axis mediated CC progression. Thus, these findings demonstrated the tumor suppressor role of miR-543 on CC progression, which might serve as a potential biomarker for CC diagnosis and therapy. |3' Untranslated Regions[MESH] |Animals[MESH] |Antagomirs/metabolism/therapeutic use[MESH] |Apoptosis[MESH] |Cell Cycle Checkpoints[MESH] |Cell Movement[MESH] |Cell Proliferation[MESH] |Female[MESH] |Humans[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |Mice, Nude[MESH] |MicroRNAs/antagonists & inhibitors/genetics/*metabolism[MESH] |Middle Aged[MESH] |Phosphatidylinositol 3-Kinases/metabolism[MESH] |Protein Serine-Threonine Kinases/chemistry/genetics/*metabolism[MESH] |Proto-Oncogene Proteins c-akt/metabolism[MESH] |Signal Transduction[MESH] |TRPM Cation Channels/chemistry/genetics/*metabolism[MESH]miR-543 inhibites cervical cancer growth and metastasis by targeting T(epmc).pdf DeepDyve Pubget Overpricing