scholarly journals Pin1 Inhibitor Juglone Exerts Anti-Oncogenic Effects on LNCaP and DU145 Cells despite the Patterns of Gene Regulation by Pin1 Differing between These Cell Lines

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0127467 ◽  
Author(s):  
Ryuhei Kanaoka ◽  
Akifumi Kushiyama ◽  
Yasuyuki Seno ◽  
Yusuke Nakatsu ◽  
Yasuka Matsunaga ◽  
...  
Keyword(s):  
Gene Regulation ◽  
Cell Lines ◽  
Pin1 Inhibitor ◽  
Du145 Cells

scholarly journals Epigenomic Analysis of RAD51 ChIP-seq Data Reveals cis-regulatory Elements Associated with Autophagy in Cancer Cell Lines

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2547
Author(s):  
Keunsoo Kang ◽  
Yoonjung Choi ◽  
Hyeonjin Moon ◽  
Chaelin You ◽  
Minjin Seo ◽  
...  
Keyword(s):  
Gene Regulation ◽  
Homologous Recombination ◽  
Cell Lines ◽  
Regulatory Elements ◽  
Binding Motif ◽  
Genome Wide ◽  
E Box ◽  
Autophagy Pathway ◽  
Mcf 7

RAD51 is a recombinase that plays a pivotal role in homologous recombination. Although the role of RAD51 in homologous recombination has been extensively studied, it is unclear whether RAD51 can be involved in gene regulation as a co-factor. In this study, we found evidence that RAD51 may contribute to the regulation of genes involved in the autophagy pathway with E-box proteins such as USF1, USF2, and/or MITF in GM12878, HepG2, K562, and MCF-7 cell lines. The canonical USF binding motif (CACGTG) was significantly identified at RAD51-bound cis-regulatory elements in all four cell lines. In addition, genome-wide USF1, USF2, and/or MITF-binding regions significantly coincided with the RAD51-associated cis-regulatory elements in the same cell line. Interestingly, the promoters of genes associated with the autophagy pathway, such as ATG3 and ATG5, were significantly occupied by RAD51 and regulated by RAD51 in HepG2 and MCF-7 cell lines. Taken together, these results unveiled a novel role of RAD51 and provided evidence that RAD51-associated cis-regulatory elements could possibly be involved in regulating autophagy-related genes with E-box binding proteins.

scholarly journals An intriguing characteristic of enhancer-promoter interactions

2020 ◽  
Author(s):  
Amlan Talukder ◽  
Haiyan Hu ◽  
Xiaoman Li
Keyword(s):  
Gene Regulation ◽  
Cell Lines ◽  
Target Genes ◽  
Cell Types ◽  
Primary Cell ◽  
Base Pairs ◽  
Distal Gene

ABSTRACTIt is still challenging to predict interacting enhancer-promoter pairs (IEPs), partially because of our limited understanding of their characteristics. To understand IEPs better, here we studied the IEPs in nine cell lines and nine primary cell types. We observed that one enhancer is likely to interact with either none or all of the target genes of another enhancer. This observation implies that enhancers form clusters, and every enhancer in the same cluster synchronously interact with almost every member of a set of genes and only this set of genes. We perceived that an enhancer can be up to two mega base pairs away from other enhancers in the same cluster. We also noticed that although a fraction of these clusters of enhancers do overlap with super-enhancers, the majority of the enhancer clusters are different from the known super-enhancers. Our study showed a new characteristic of IEPs, which may shed new light on distal gene regulation and the identification of IEPs.

scholarly journals Up-Regulation of LINC00665 Facilitates the Malignant Progression of Prostate Cancer by Epigenetically Silencing KLF2 Through EZH2 and LSD1

2021 ◽  
Vol 11 ◽  
Author(s):  
Peng Xue ◽  
Miao Yan ◽  
Kunpeng Wang ◽  
Jinbao Gu ◽  
Bing Zhong ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Lines ◽  
Malignant Progression ◽  
Expression Level ◽  
Regulation Mechanism ◽  
Knock Down ◽  
Qrt Pcr ◽  
Mouse Xenograft Model ◽  
Du145 Cells

This study aimed to explore the function of LINC00665 on the proliferation and metastasis of prostate cancer (PCa), and the potential regulatory mechanisms were also investigated. The expression level of LINC00665 in 50 pairs of PCa tissues and adjacent ones was studied by qRT-PCR, and the associations between LINC00665 and clinicopathological characteristics of PCa patients were analyzed. Control group (sh-NC) and LINC00665 knock-down group (sh-LINC00665) were set in 22RV1 and DU145 cells, respectively. The biological functions of LINC00665 in PCa cell lines were assessed by CCK-8, EdU, Transwell assays, and the nude mouse xenograft model was used to evaluate the tumorigenicity in vivo. In addition, qRT-PCR, Western Blot, RIP and ChIP assays were also used to determine the regulation mechanism of LINC00665 in PCa cell lines. In this study, our results showed that LINC00665 expression level in PCa cancer tissues was significantly up-regulated, compared with that in adjacent ones. Besides, similar results were found in PCa cell lines. Knock-down of LINC00665 significantly attenuated the proliferation and migration ability in 22RV1 and DU145 cells, compared to sh-NC. Mechanically, LINC00665 could interact with EZH2 and LSD1, recruiting them to KLF2 promoter region to inhibit its transcription. Moreover, the tumor-suppressive effects mediated by sh-LINC00665 were significantly reversed through the down-regulation of KLF2. Also, the suppression of LINC00665 impaired tumor growth of PCa in vivo. In summary, LINC00665 exerted the oncogenic functions in PCa cell lines by epigenetically silencing KLF2 expression by binding to EZH2 and LSD1, illuminating a novel mechanism of LINC00665 in the malignant progression of PCa and furnishing a prospective therapeutic biomarker to combat PCa.

scholarly journals Landscape of electrophilic and inflammatory stress-mediated gene regulation in human lymphoblastoid cell lines

2020 ◽  
Vol 161 ◽  
pp. 71-83
Author(s):  
Noriko Ishida ◽  
Yuichi Aoki ◽  
Fumiki Katsuoka ◽  
Ichiko Nishijima ◽  
Takahiro Nobukuni ◽  
...  
Keyword(s):  
Gene Regulation ◽  
Cell Lines ◽  
Lymphoblastoid Cell Lines ◽  
Inflammatory Stress ◽  
Human Lymphoblastoid Cell ◽  
Human Lymphoblastoid Cell Lines

scholarly journals Activation of the Y1 Receptor by Neuropeptide Y Regulates the Growth of Prostate Cancer Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1466-1473 ◽  
Author(s):  
Massimiliano Ruscica ◽  
Elena Dozio ◽  
Stéphane Boghossian ◽  
Giorgio Bovo ◽  
Vera Martos Riaño ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Neuropeptide Y ◽  
Cell Lines ◽  
Y1 Receptor ◽  
Intracellular Signals ◽  
Relevant Role ◽  
Pc3 Cells ◽  
Du145 Cells ◽  
Kinetics Of

This study deals with the role of neuropeptide Y (NPY) in the regulation of cell proliferation. NPY is expressed in the normal and tumoral prostate, but no data on its possible role in prostate cancer (PCa) progression are available. Therefore, we evaluated the direct effect of NPY on the growth of the human PCa cell lines LNCaP (androgen dependent) and DU145 and PC3 (androgen independent). All PCa cell lines expressed Y1-R gene and protein. NPY treatment reduced the proliferation of LNCaP and DU145 cells and increased that of PC3 cells. The Y1-R antagonist BIBP3226 abolished such effects, suggesting a mandatory role of Y1-R in this process. LNCaP cells showed elevated constitutive levels of phosphorylated ERK1/2, which were not affected by NPY. In DU145 cells, NPY stimulated a long-lasting ERK1/2 activation, whereas, in PC3 cells, this effect was rapid and transient and required activation of protein kinase C. Moreover, in both cell lines, pretreatment with BIBP3226 prevented the NPY-induced ERK1/2 phosphorylation, further supporting Y1-R involvement. NPY treatment reduced forskolin-stimulated cAMP accumulation only in PC3 cells and did not change intracellular calcium concentration in any PCa cell line. These data indicate that NPY may directly regulate PCa cell growth via Y1-R. The direction of this effect appears to be related to the time kinetics of MAPK activation, i.e. long-lasting vs. transient, and to the clone-specific involvement of other intracellular signals. These findings suggest that NPY-related mechanisms might play a relevant role in the progression of PCa, at both androgen dependent and independent stages.

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