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10.1155/2020/6724810 http://scihub22266oqcxt.onion/10.1155/2020/6724810 32215176!7079255!32215176     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32215176&cmd=llinks): Failed to open stream: HTTP request failed! 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Suppression of TRPM7 Inhibited Hypoxia-Induced Migration and Invasion of Androgen-Independent Prostate Cancer Cells by Enhancing RACK1-Mediated Degradation of HIF-1alpha |pdf=|usr=}}{{32215176}} gab.com Text Suppression of TRPM7 Inhibited Hypoxia-Induced Migration and Invasion of Androgen-Independent Prostate Cancer Cells by Enhancing RACK1-Mediated Degradation of HIF-1alpha JO: Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=32215176 #FOAvip Transient receptor potential melastatin subfamily member 7 (TRPM7) was essential in the growth and metastatic ability of prostate cancer cells. However, the effects and the relevant molecular mechanisms of TRPM7 on metastasis of prostate cancer under hypoxic atmosphere remain unclear. This study investigated the role of TRPM7 in the metastatic ability of androgen-independent prostate cancer cells under hypoxia. First, data mining was carried out to disclose the relationship between the TRPM7 gene level and the survival of prostate cancer patients. Specific siRNAs were used to knockdown target genes. Western blotting and qPCR were employed to determine protein and gene expression, respectively. The gene transcription activity was evaluated by luciferase activity assay of promoter gene. The protein interaction was determined by coimmunoprecipitation. Wound healing and transwell assays were employed to evaluated cell migration and invasion, respectively. Open access database results showed that high expression of TRPM7 was closely related to the poor survival of prostate cancer patients. Hypoxia simultaneously increased TRPM7 expression and induced HIF-1alpha accumulation in androgen-independent prostate cancer cells. Knockdown of TRPM7 significantly promoted HIF-1alpha degradation through the proteasome and inhibited EMT changes in androgen-independent prostate cancer cells under hypoxic condition. Moreover, TRPM7 knockdown increased the phosphorylation of RACK1 and strengthened the interaction between RACK1 and HIF-1alpha but attenuated the binding of HSP90 to HIF-1alpha. Whereas knockdown of RACK1 increased the binding of HSP90 to HIF-1alpha. Furthermore, both TRPM7 and HIF-1alpha knockdown significantly suppressed hypoxia-induced Annexin A1 protein expression, and suppression of HIF-1alpha/Annexin A1 signaling significantly inhibited hypoxia-induced cell migration and invasion of androgen-independent prostate cancer cells. Our findings demonstrate that TRPM7 knockdown promotes HIF-1alpha degradation via an oxygen-independent mechanism involving increased binding of RAKC1 to HIF-1alpha, and TRPM7-HIF-1alpha-Annexin A1 signaling axis plays a crucial role in the EMT, cell migration, and invasion of androgen-independent prostate cancer cells under hypoxic conditions. Twit Text FOAVip Suppression of TRPM7 Inhibited Hypoxia-Induced Migration and Invasion of Androgen-Independent Prostate Cancer Cells by Enhancing RACK1-Mediated Degradation of HIF-1alpha ????Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=32215176 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32215176 #FOAvip English Wikipedia <ref>{{Cite pmid|32215176}}</ref> Suppression of TRPM7 Inhibited Hypoxia-Induced Migration and Invasion of Androgen-Independent Prostate Cancer Cells by Enhancing RACK1-Mediated Degradation of HIF-1alpha #MMPMID32215176 Yang F; Cai J; Zhan H; Situ J; Li W; Mao Y; Luo Y Oxid Med Cell Longev 2020[]; 2020 (ä): 6724810 PMID32215176show ga Transient receptor potential melastatin subfamily member 7 (TRPM7) was essential in the growth and metastatic ability of prostate cancer cells. However, the effects and the relevant molecular mechanisms of TRPM7 on metastasis of prostate cancer under hypoxic atmosphere remain unclear. This study investigated the role of TRPM7 in the metastatic ability of androgen-independent prostate cancer cells under hypoxia. First, data mining was carried out to disclose the relationship between the TRPM7 gene level and the survival of prostate cancer patients. Specific siRNAs were used to knockdown target genes. Western blotting and qPCR were employed to determine protein and gene expression, respectively. The gene transcription activity was evaluated by luciferase activity assay of promoter gene. The protein interaction was determined by coimmunoprecipitation. Wound healing and transwell assays were employed to evaluated cell migration and invasion, respectively. Open access database results showed that high expression of TRPM7 was closely related to the poor survival of prostate cancer patients. Hypoxia simultaneously increased TRPM7 expression and induced HIF-1alpha accumulation in androgen-independent prostate cancer cells. Knockdown of TRPM7 significantly promoted HIF-1alpha degradation through the proteasome and inhibited EMT changes in androgen-independent prostate cancer cells under hypoxic condition. Moreover, TRPM7 knockdown increased the phosphorylation of RACK1 and strengthened the interaction between RACK1 and HIF-1alpha but attenuated the binding of HSP90 to HIF-1alpha. Whereas knockdown of RACK1 increased the binding of HSP90 to HIF-1alpha. Furthermore, both TRPM7 and HIF-1alpha knockdown significantly suppressed hypoxia-induced Annexin A1 protein expression, and suppression of HIF-1alpha/Annexin A1 signaling significantly inhibited hypoxia-induced cell migration and invasion of androgen-independent prostate cancer cells. Our findings demonstrate that TRPM7 knockdown promotes HIF-1alpha degradation via an oxygen-independent mechanism involving increased binding of RAKC1 to HIF-1alpha, and TRPM7-HIF-1alpha-Annexin A1 signaling axis plays a crucial role in the EMT, cell migration, and invasion of androgen-independent prostate cancer cells under hypoxic conditions. |Annexin A1/genetics/metabolism[MESH] |Cell Line, Tumor[MESH] |Cell Movement[MESH] |Epithelial-Mesenchymal Transition[MESH] |Gene Expression Regulation, Neoplastic[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism[MESH] |Male[MESH] |Neoplasm Proteins/*metabolism[MESH] |Phosphorylation[MESH] |Prognosis[MESH] |Prostatic Neoplasms, Castration-Resistant/genetics/metabolism/*pathology[MESH] |Proteasome Endopeptidase Complex/metabolism[MESH] |Protein Binding[MESH] |Protein Serine-Threonine Kinases/*genetics/metabolism[MESH] |Receptors for Activated C Kinase/*metabolism[MESH] |Signal Transduction[MESH] |TRPM Cation Channels/*genetics/metabolism[MESH]Suppression of TRPM7 Inhibited Hypoxia-Induced Migration and Invasion (epmc).pdf DeepDyve Pubget Overpricing