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activates igf-1r/pi3k/akt signaling cytokine-mediated islet stress month download article/chapter assessing high-risk factors paraffin-embedded canine meningioma microrna-132/nrf2 axis rna-seq transcriptome analysis full article pdf nedd4 ubiquitin ligase ubiquitin-protein ligases privacy choices/manage cookies immune cell infiltration upstream gene nedd4 ubiquitination research published national key research nedd4 degrades tusc2 nedd4 facilitates ishikawa cell suspensions child healthcare hospital holds exclusive rights promote glioblastoma progression article guo pamr1 overexpression suppressed immune-related genes low pamr1 expression european economic area check access mtor/4ebp1 activation microarray data analysis microrna-340-5p suppression ying yuan laboratory animals issued electronic supplementary material instant access nedd4 regulates ubiquitination glycosyltransferase-related prognostic southern medical university article number 65 article log conditions privacy policy 17-gene prognosis signature endometrial carcinoma epithelial malignant neoplasm accepted manuscript version tumor xenograft model diagnostic prognostic marker article cite integrative analysis accepting optional cookies additional information publisher

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         headline:NEDD4 facilitates the progression of endometrial carcinoma by enhancing PAMR1 protein degradation through ubiquitination
         description:Endometrial carcinoma (EC) is an epithelial malignant neoplasm that frequently appears in postmenopausal and perimenopausal women. PAMR1 is related to the prognosis of EC. Here, we probed into the significance of PAMR1 in EC progression and its acting mechanism. In silico analysis was conducted to identify the differentially expressed gene PAMR1 and its upstream gene NEDD4 in EC, followed by the determination of their expression in EC tissues and cells. The gene expression, cell proliferation, angiogenesis, migration, invasion, and apoptosis were examined after ectopic expression or knockdown experiments. The interaction between NEDD4 and PAMR1 and the level of PAMR1 ubiquitination were examined. The injection of Ishikawa cell suspensions into nude mice was carried out to establish a tumor xenograft model, validating the roles of PAMR1 and NEDD4 in EC. EC cells exhibited high NEDD4 expression and low PAMR1 expression. NEDD4 knockdown or PAMR1 overexpression suppressed the invasive, migrating, angiogenic, and proliferative properties of EC cells while promoting apoptosis. NEDD4 facilitated PAMR1 protein degradation through ubiquitination. Deletion of PAMR1 abolished the inhibitory effects of NEDD4 knockdown on the malignant behaviors of EC cells. Furthermore, NEDD4 knockdown restrained EC growth in nude mice by increasing PAMR1 protein expression. NEDD4 facilitated EC progression by enhancing PAMR1 protein degradation through ubiquitination.
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      headline:NEDD4 facilitates the progression of endometrial carcinoma by enhancing PAMR1 protein degradation through ubiquitination
      description:Endometrial carcinoma (EC) is an epithelial malignant neoplasm that frequently appears in postmenopausal and perimenopausal women. PAMR1 is related to the prognosis of EC. Here, we probed into the significance of PAMR1 in EC progression and its acting mechanism. In silico analysis was conducted to identify the differentially expressed gene PAMR1 and its upstream gene NEDD4 in EC, followed by the determination of their expression in EC tissues and cells. The gene expression, cell proliferation, angiogenesis, migration, invasion, and apoptosis were examined after ectopic expression or knockdown experiments. The interaction between NEDD4 and PAMR1 and the level of PAMR1 ubiquitination were examined. The injection of Ishikawa cell suspensions into nude mice was carried out to establish a tumor xenograft model, validating the roles of PAMR1 and NEDD4 in EC. EC cells exhibited high NEDD4 expression and low PAMR1 expression. NEDD4 knockdown or PAMR1 overexpression suppressed the invasive, migrating, angiogenic, and proliferative properties of EC cells while promoting apoptosis. NEDD4 facilitated PAMR1 protein degradation through ubiquitination. Deletion of PAMR1 abolished the inhibitory effects of NEDD4 knockdown on the malignant behaviors of EC cells. Furthermore, NEDD4 knockdown restrained EC growth in nude mice by increasing PAMR1 protein expression. NEDD4 facilitated EC progression by enhancing PAMR1 protein degradation through ubiquitination.
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         Endometrial carcinoma
         NEDD4
         PAMR1
         Ubiquitination
         Cell Biology
         Plant Genetics and Genomics
         Microbial Genetics and Genomics
         Biochemistry
         general
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         Animal Genetics and Genomics
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PostalAddress:
      name:Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Women and Children’s Medical Center, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Women and Children’s Medical Center, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Women and Children’s Medical Center, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Women and Children’s Medical Center, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Women and Children’s Medical Center, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Women and Children’s Medical Center, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Department of Ultrasound, Affiliated Hospital of Guilin Medical University, Guilin, China
      name:Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Women and Children’s Medical Center, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China
      name:Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China
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