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NR5A2 transcriptional activation by BRD4 promotes pancreatic cancer progression by upregulating GDF15
by
Zhou Yingke
, Guo, Feng
, Ren Dianyun
, Jin, Xin
, Wu Heshui
, Guo, Hui
in
Adenocarcinoma
/ Cell proliferation
/ Chromatin
/ Gene expression
/ Immunohistochemistry
/ Immunoprecipitation
/ Malignancy
/ Pancreatic cancer
/ Transcription activation
/ Transcriptomes
/ Western blotting
/ Wound healing
2021
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NR5A2 transcriptional activation by BRD4 promotes pancreatic cancer progression by upregulating GDF15
by
Zhou Yingke
, Guo, Feng
, Ren Dianyun
, Jin, Xin
, Wu Heshui
, Guo, Hui
in
Adenocarcinoma
/ Cell proliferation
/ Chromatin
/ Gene expression
/ Immunohistochemistry
/ Immunoprecipitation
/ Malignancy
/ Pancreatic cancer
/ Transcription activation
/ Transcriptomes
/ Western blotting
/ Wound healing
2021
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While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
NR5A2 transcriptional activation by BRD4 promotes pancreatic cancer progression by upregulating GDF15
by
Zhou Yingke
, Guo, Feng
, Ren Dianyun
, Jin, Xin
, Wu Heshui
, Guo, Hui
in
Adenocarcinoma
/ Cell proliferation
/ Chromatin
/ Gene expression
/ Immunohistochemistry
/ Immunoprecipitation
/ Malignancy
/ Pancreatic cancer
/ Transcription activation
/ Transcriptomes
/ Western blotting
/ Wound healing
2021
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NR5A2 transcriptional activation by BRD4 promotes pancreatic cancer progression by upregulating GDF15
Journal Article
NR5A2 transcriptional activation by BRD4 promotes pancreatic cancer progression by upregulating GDF15
2021
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Overview
NR5A2 is a transcription factor regulating the expression of various oncogenes. However, the role of NR5A2 and the specific regulatory mechanism of NR5A2 in pancreatic ductal adenocarcinoma (PDAC) are not thoroughly studied. In our study, Western blotting, real-time PCR, and immunohistochemistry were conducted to assess the expression levels of different molecules. Wound-healing, MTS, colony formation, and transwell assays were employed to evaluate the malignant potential of pancreatic cancer cells. We demonstrated that NR5A2 acted as a negative prognostic biomarker in PDAC. NR5A2 silencing inhibited the proliferation and migration abilities of pancreatic cancer cells in vitro and in vivo. While NR5A2 overexpression markedly promoted both events in vitro. We further identified that NR5A2 was transcriptionally upregulated by BRD4 in pancreatic cancer cells and this was confirmed by Chromatin immunoprecipitation (ChIP) and ChIP-qPCR. Besides, transcriptome RNA sequencing (RNA-Seq) was performed to explore the cancer-promoting effects of NR5A2, we found that GDF15 is a component of multiple down-regulated tumor-promoting gene sets after NR5A2 was silenced. Next, we showed that NR5A2 enhanced the malignancy of pancreatic cancer cells by inducing the transcription of GDF15. Collectively, our findings suggest that NR5A2 expression is induced by BRD4. In turn, NR5A2 activates the transcription of GDF15, promoting pancreatic cancer progression. Therefore, NR5A2 and GDF15 could be promising therapeutic targets in pancreatic cancer.
Publisher
Springer Nature B.V
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