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WNT11 is a direct target of early growth response protein 1
JuHwan Kim1 (Graduate student), Euitaek Jung1 (Graduate student), Sung Shin Ahn1 (Graduate student), Hyunjin Yeo 1 (Graduate student), Jeong Yeon Lee 1 (Graduate student), Jeong Kon Seo2 (Professor), Young Han Lee Lee1 (Professor), SoonYoung Shin 1,* (Professor)
1Department of Biological Sciences, Koknkuk University,
2Central Research Facilities, Ulsan National Institute of Science and Technology
WNT11 is a member of the non-canonical Wnt family and plays a crucial role in tumor progression. However, the regulatory mechanisms underlying WNT11 expression are unclear. Tumor necrosis factor-alpha (TNFメ) is a major inflammatory cytokine produced in the tumor microenvironment and contributes to processes associated with tumor progression, such as tumor invasion and metastasis. By using site-directed mutagenesis and introducing a serial deletion in the 5'-regulatory region of WNT11, we observed that TNFメ activates the early growth response 1 (EGR1)-binding sequence (EBS) in the proximal region of WNT11 and that the transcription factor EGR1 is necessary for the TNFメ-induced transcription of WNT11. EGR1 bound directly to the EBSs within the proximal 5'-regulatory region of WNT11 and ectopic expression of EGR1 stimulated WNT11 promoter activity, whereas the knockdown of EGR1 expression by RNA interference reduced TNFメ-induced WNT11 expression in T47D breast cancer cells. We also observed that mitogen-activated protein kinases (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 kinase mediated TNFメ-induced transcription of WNT11 via EGR1. Our results suggest that EGR1 directly targets WNT11 in response to TNFメ stimulation in breast cancer cells.
Abstract, Accepted Manuscript(in press) [Submitted on March 9, 2020, Accepted on July 6, 2020]
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