Abstract:NF45, also referred to as nuclear factor of activated T cells, has been reported to promote the progression of multiple cancer types. However, the expression and physiological significance of NF45 in pancreatic ductal adenocarcinoma (PDAC) remain largely elusive. In this study, we investigated the clinical relevance and potential role of NF45 expression in PDAC development. Western blot analysis revealed that NF45 was remarkably upregulated in PDAC tissues, compared with the adjacent non-tumorous ones. In addi… Show more
“…It has been reported that ILF2 is abundantly expressed in pancreatic carcinoma (8) and it functions as an oncogene. Thus, we aimed to elucidate the mechanisms underlying the increased ILF2 expression in pancreatic carcinoma.…”
Section: Resultsmentioning
confidence: 99%
“…Thus, ILF2 may be a potential therapeutic target (8). Yet, the regulatory mechanisms of ILF2 remain largely elusive.…”
Section: Discussionmentioning
confidence: 99%
“…We found that miR-7 suppressed ILF2 protein expression and inhibited the proliferation, colony formation, migration and invasion as well as negatively regulated EMT-associated gene expression in PANC-1 cells. It has been reported that ILF2 is markedly upregulated in pancreatic carcinoma (8). Our results further demonstrated that miR-7 was significantly downregulated in pancreatic tissues, implying that ILF2 upregulation may be due to the lack of miR-7.…”
Section: Discussionmentioning
confidence: 99%
“…ILF2 is ubiquitously expressed in human tissues, especially the brain, thymus, pancreas, kidney and testis indicating that it is involved in the physiology of various cell types (4). ILF2 has been reported to promote the progression of multiple cancer types including cervical cancer, esophageal squamous cell carcinoma, glioma, pancreatic carcinoma and non-small cell lung cancer (5–8). Yet, the regulatory mechanisms of ILF2 remain largely elusive.…”
Interleukin enhancer binding factor 2 (ILF2) has been found to be markedly upregulated in pancreatic carcinoma and is involved in the pathogenesis of pancreatic carcinoma. Thus, ILF2 may be a potential target for therapy. Yet, the regulatory mechanisms of ILF2 in pancreatic carcinoma remain largely elusive. In the present study, we demonstrated that ILF2 functioned as an oncogene and regulated epithelial-mesenchymal transition (EMT)-associated genes in pancreatic carcinoma PANC-1 cells. MicroRNA-7 (miR-7) suppressed ILF2 mRNA expression and the protein level in PANC-1 cells. Contrary to ILF2, miRNA-7 functioned as a tumor-suppressor gene and negatively regulated EMT-associated genes in the PANC-1 cells. Curcumin, a polyphenol natural product isolated from the rhizome of the plant Curcuma longa, has emerged as a promising anticancer therapeutic agent. We found that treatment with curcumin increased miR-7 expression and suppressed ILF2 protein in the PANC-1 cells. Thus, we identified ILF2 as a new downstream target gene of curcumin. The results revealed that ILF2 is regulated by miR-7 and suggest that downregulation of miR-7 may be an important factor for the ILF2 overexpression in pancreatic carcinoma.
“…It has been reported that ILF2 is abundantly expressed in pancreatic carcinoma (8) and it functions as an oncogene. Thus, we aimed to elucidate the mechanisms underlying the increased ILF2 expression in pancreatic carcinoma.…”
Section: Resultsmentioning
confidence: 99%
“…Thus, ILF2 may be a potential therapeutic target (8). Yet, the regulatory mechanisms of ILF2 remain largely elusive.…”
Section: Discussionmentioning
confidence: 99%
“…We found that miR-7 suppressed ILF2 protein expression and inhibited the proliferation, colony formation, migration and invasion as well as negatively regulated EMT-associated gene expression in PANC-1 cells. It has been reported that ILF2 is markedly upregulated in pancreatic carcinoma (8). Our results further demonstrated that miR-7 was significantly downregulated in pancreatic tissues, implying that ILF2 upregulation may be due to the lack of miR-7.…”
Section: Discussionmentioning
confidence: 99%
“…ILF2 is ubiquitously expressed in human tissues, especially the brain, thymus, pancreas, kidney and testis indicating that it is involved in the physiology of various cell types (4). ILF2 has been reported to promote the progression of multiple cancer types including cervical cancer, esophageal squamous cell carcinoma, glioma, pancreatic carcinoma and non-small cell lung cancer (5–8). Yet, the regulatory mechanisms of ILF2 remain largely elusive.…”
Interleukin enhancer binding factor 2 (ILF2) has been found to be markedly upregulated in pancreatic carcinoma and is involved in the pathogenesis of pancreatic carcinoma. Thus, ILF2 may be a potential target for therapy. Yet, the regulatory mechanisms of ILF2 in pancreatic carcinoma remain largely elusive. In the present study, we demonstrated that ILF2 functioned as an oncogene and regulated epithelial-mesenchymal transition (EMT)-associated genes in pancreatic carcinoma PANC-1 cells. MicroRNA-7 (miR-7) suppressed ILF2 mRNA expression and the protein level in PANC-1 cells. Contrary to ILF2, miRNA-7 functioned as a tumor-suppressor gene and negatively regulated EMT-associated genes in the PANC-1 cells. Curcumin, a polyphenol natural product isolated from the rhizome of the plant Curcuma longa, has emerged as a promising anticancer therapeutic agent. We found that treatment with curcumin increased miR-7 expression and suppressed ILF2 protein in the PANC-1 cells. Thus, we identified ILF2 as a new downstream target gene of curcumin. The results revealed that ILF2 is regulated by miR-7 and suggest that downregulation of miR-7 may be an important factor for the ILF2 overexpression in pancreatic carcinoma.
“…disruption of NF90 and NF45 impaired ESC proliferation and promoted differentiation to an epiblast-like state (27). NF90 and NF45 regulate cell cycle progression (18,19,28), cell growth and proliferation (28)(29)(30)(31)(32)(33), and are amplified, overexpressed and mutated in diverse cancers (34,35).…”
Immediate early gene (IEG) transcription is rapidly activated by diverse stimuli without requiring new protein synthesis. This transcriptional regulation is assumed to involve constitutively expressed nuclear factors that are targets of signaling cascades initiated at the cell membrane. NF45 and its heterodimeric partner NF90 are chromatin-interacting proteins that are constitutively expressed and localized predominantly in the nucleus. Previously, NF90 chromatin immunoprecipitation followed by deep sequencing (ChIP-seq)
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