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ChIP-seq analysis
Published in Altuna Akalin, Computational Genomics with R, 2020
The motif shown in Figure 9.22 corresponds to the previously visualized CTCF motif. Nevertheless, we will computationally annotate our motif by querying the JASPAR (Khan et al., 2018) database in the next section.
The anterior thalamus and the pentylenetetrazol (PTZ) model
Published in Hans O Lüders, Deep Brain Stimulation and Epilepsy, 2020
Marek A Mirski, David L Sherman, Wendy C Ziai
The expression of such generalized or partial-complex seizures appears to result from disturbances in multiple anatomical systems of brain occurring in a synchronous fashion.12–24 Since the early days of electroencephalography and deep brain recording, it was postulated that both forebrain and subcortical influences appeared to be important in the development of EEG and behavioral con-vulsant activity. Early support was derived from the works by Morison et al. and Dempsey and Morison that demonstrated the existence of diffuse projection channels linking the brainstem to the entire cortex.25,26Through such paths, epileptic cortical generalized discharges could be triggered from the brainstem. Three cycle per second spike-wave complexes were elicited on cortical EEG, resembling the epileptiform discharges seen in human petit mal epilepsy. These complexes were produced by stimulating the cat anterior thalamus and intralaminar nuclei with electrical pulses of the same frequency. This concept was soon to be coined the ‘centroencephalic’ theory by Penfield and Jaspar.27
Transcription factor ETV1-induced lncRNA MAFG-AS1 promotes migration, invasion, and epithelial–mesenchymal transition of pancreatic cancer cells by recruiting IGF2BP2 to stabilize ETV1 expression
Published in Growth Factors, 2023
Hanqin Weng, Weijian Feng, Fengling Li, Dong Huang, Liangyi Lin, Zaiguo Wang
Subsequently, the protein expression levels of ETV1 in normal HPNE cells and PC cells (AsPC-1 cell line) were determined by WB, which illustrated that compared with HPNE cells, ETV1 in PC cell line AsPC-1 was raised (p < .05) (Figure 2(A)). Through the JASPAR website (http://jaspar.genereg.net/), we found five binding sites between the MAFG-AS1 promoter region and ETV1 (Figure 2(B,C)). Furthermore, to figure out the specific interaction location between them, we conducted dual-luciferase assay and discovered that overexpression of ETV1 caused an elevation in the luciferase activity of the MAFG-AS1 promoter of wild-type or with mutation at site 1/2/4/5 in AsPC-1 cells, while no distinct changes were observed in MAFG-AS1 promoter at site 3 and all five mutated sites (Figure 2(D)), suggesting that ETV1 bound to site 3 of the MAFG-AS1 promoter. ChIP analysis uncovered that the fragment of the MAFG-AS1 promoter region, rather than the MAFG-AS1 gene region, was highly enriched in anti-ETV1 groups (Figure 2(E)), indicating a specific combination between the MAFG-AS1 promoter and ETV1 in PC cells. In addition, we overexpressed ETV1 in AsPC-1 cells, and RT-qPCR showed the increased level of ETV1 (p < .05) (Figure 2(F)). Further, the expression of MAFG-AS1 was also significantly increased after overexpression of ETV1 (p < .05) (Figure 2(G)). We concluded that ETV1 can induce MAFG-AS1 transcription in PC cells.
ANLN, Regulated by SP2, Promotes Colorectal Carcinoma Cell Proliferation via PI3K/AKT and MAPK Signaling Pathway
Published in Journal of Investigative Surgery, 2022
Yanwei Liu, Pengwei Cao, Feng Cao, Song Wang, Yan He, Yanyan Xu, Yong Wang
Transcription factors are gene regulators that recognize specific DNA sequences, bind chromatin, and form a complex that transcriptionally regulates the expression of genes [15]. We used bioinformatics tools based on JASPAR to predict the potential transcription factors that may regulate ANLN, and SP2 was strongly suggested as a regulator of ANLN according to the putative score. SP2 is a multifunctional transcription factor and cancer promoter in multiple tumors [13,14]. Our study results are consistent with these reports. SP2 depletion by targeted siRNA led to reduced levels of ANLN mRNA, which implied that ANLN-mediated control of CRC cell progression may be transcriptionally regulated by SP2. However, other external factors may be involved in ANLN regulation, such as the tumor microenvironment, and these potential regulatory elements require further investigation.
SP1-induced up-regulation of lncRNA LUCAT1 promotes proliferation, migration and invasion of cervical cancer by sponging miR-181a
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Liang Zhang, Shi-Kai Liu, Lili Song, Hai-Rong Yao
Up to date, although more and more lncRNAs were confirmed to be abnormally expressed in various tumours, including CC, the critical factors involved in their altered expression pattern in tumours are still not well understood. Recently, growing data indicated that the levels of lncRNAs can be modulated by transcription factors and epigenetic regulators [26,27]. For instance, SP1-induced overexpression of lncRNA SNHG14 could contribute to the progression of clear cell renal cell carcinoma [28]. SP1 activates lncRNA UCA1 transcription to promote gastric cancer cells proliferation via recruiting EZH2 [29]. In this study, via analyzing the JASPAR CORE database, we focused on SP1 transcription factor because there are several SP1 binding sites in the promoter region of LUCAT1 and the roles of SP1 have been studied in CC. Then, we down-regulated the expression of SP1 and performed luciferase reporter assays and ChIP, confirming that SP1 could physically interact with the promoter of LUCAT1. In addition, we found that overexpression of SP1 promoted LUCAT1 expression, whereas down-regulation of SP1 suppressed LUCAT1 expression. Thus, our findings indicated that the expression of LUCAT1 may be modulated by SP1.