Molecular Characterization, Expression Patterns, and Association Analysis with Carcass Traits of Porcine USF1 Gene

Wu, Huayu; Qiao, Mu; Peng, Xianwen; Wu, Jianliang; Liu, Guisheng; Sun, Hua; Li, Lianghua; Mei, Shuqi

doi:10.1007/s12010-013-0280-5

Cited by 12 publications

(11 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As an important regulatory factor, USF has highly conserved bHLH-LZ domain and binds to consensus sequence (CANNTG) of E-box to further regulate the transcription process of different proteins (Wu et al, 2013; Lupp et al, 2014). USF1 was reported to regulate the expression of IL-10 in glioma related microglia: inhibition of USF1 expression resulted in the up-regulation of IL-10 expression (Zhang et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB

Zhao

et al. 2017

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Homeobox transcript antisense intergenic RNA (HOTAIR), as a long non-coding RNA (lncRNA), has been considered to play critical roles in the biological properties of various tumors. The purposes of this study were to investigate the role and possible molecular mechanisms of HOTAIR in regulating the permeability of blood tumor barrier (BTB) in vitro. Our present study elucidated that the expressions of HOTAIR and upstream stimulatory factor 1 (USF1) was up-regulated, but miR-148b-3p was down-regulated in glioma microvascular endothelial cells (GECs). Knockdown of HOTAIR could increase the permeability of BTB as well as down-regulated the expressions of tight junction related proteins ZO-1, occludin, claudin-5, but up-regulated miR-148b-3p expressions in GECs. Meanwhile, dual-luciferase reporter assays demonstrated that HOTAIR was a target RNA of miR-148b-3p. Furthermore, overexpression of miR-148b-3p increased the permeability of BTB by down-regulating the expressions of tight junction related proteins and USF1 in GECs, and vice versa. And further result revealed USF1 was a target of miR-148b-3p. Silence of USF1 increased the permeability of BTB duo to their interaction with the promoters of ZO-1, occludin, and claudin-5 in GECs. Taken together, our finding indicated that knockdown of HOTAIR increased BTB permeability via binding to miR-148b-3p, which further reducing tight junction related proteins in GECs by targeting USF1. Thus, HOTAIR will attract more attention since it can serve as a potential target of drug delivery across BTB and may provide novel strategies for glioma treatment.

show abstract

Section: Introductionmentioning

confidence: 99%

RETRACTED: The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB

Zhao

et al. 2017

Front. Mol. Neurosci.

View full text Add to dashboard Cite

show abstract

“…The human upstream transcription factor 1 (USF1) gene is located in the q22.3 region of chromosome 1. USF1 contains an HLH-LZ structure (helix-loop-helix leucine zipper) that can bind to the E-box of various gene promoter regions 12 and is involved in regulating genes related to lipid and carbohydrate homeostasis in the human body 13 . During DNA damage, USF1 can stabilize the p53 protein and briefly halt the cell cycle 14 .…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis

Wang

Zheng

Liu

et al. 2019

Molecular Therapy - Nucleic Acids

View full text Add to dashboard Cite

The anti-angiogenic treatment of malignant glioma cells is an effective method to treat high-grade gliomas. However, due to the presence of vasculogenic mimicry (VM), the anti-angiogenic treatment of gliomas is not significantly effective in improving overall patient median survival. Therefore, this study investigated the mechanism of mimic formation of angiogenesis in gliomas. The results of this experiment indicate that the expression of upstream transcription factor 1 (USF1) is upregulated in glioma tissues and cells. USF1 knockdown inhibits the proliferation, migration, invasion, VM, and expression of VM-associated proteins in glioma cells by stimulating SNHG16 and linc00667. These two long non-coding RNAs (lncRNAs) regulate ALHD1A1 through the competing endogenous RNA (ceRNA) mechanism influencing the VM of glioma. This study is the first to demonstrate that the USF1/SNHG16/miR-212-3p/ALDH1A1 (aldehyde dehydrogenase-1) and USF1/linc00667/miR-429/ALDH1A1 axis regulates the VM of glioma cells, and these findings might provide a novel strategy for glioma treatment.

show abstract

“…Upstream stimulating factor 1 (USF1) is a critical component of the basic helix-loop-helix leucine zipper (bHLH-LZ) family of transcription factors. 35 The HLH-LZ structure contained in USF1 can combine with the E-box of many gene promoter regions. 36 Therefore, USF1 involves in the transcription process of numerous proteins and works as an important regulatory factor in plenty of diseases, including cancer.…”

Section: Discussionmentioning

confidence: 99%

LncRNA LOXL1‐AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR‐708‐5p/USF1 pathway

Sun

Фан

et al. 2019

Cell Proliferation

View full text Add to dashboard Cite

Objectives As one of the most life‐threatening malignancies, gastric cancer is the third contributor of cancer mortalities globally. Increasing studies have proven the regulatory roles of lncRNAs in the development of diverse malignant tumours. But little is known about its function and molecular mechanism in gastric carcinoma. Materials and methods RT‐qPCR was performed to measure the expression pattern of LOXL1‐AS1 in gastric cancer. To ascertain its definite role, CCK‐8, EdU, Western blot, transwell and sphere formation assays were adopted. RNA pull‐down, RIP, ChIP and luciferase reporter assays were carried out to investigate the molecular mechanism of LOXL1‐AS1 in gastric carcinoma. Results LOXL1‐AS1 was highly expressed in tissues and cells of gastric cancer. The upregulation of LOXL1‐AS1 predicted poor prognosis in gastric carcinoma. Our findings demonstrated that LOXL1‐AS1 accelerated the deterioration of gastric cancer by inducing cell proliferation, migration, EMT and stemness. Moreover, the expression of USF1 in gastric cancer was higher than in normal control and LOXL1‐AS1 negatively modulated USF1. Functionally, LOXL1‐AS1 acted as a ceRNA to upregulate USF1 via sponging miR‐708‐5p. Besides, we confirmed USF1 promoted the transcription of stemness marker SOX2. Rescue experiments testified the stimulative role of LOXL1‐AS1/miR‐708‐5p/USF1 pathway in gastric cancer progression. It was also validated that LOXL1‐AS1 facilitated cell growth of gastric carcinoma in vivo. Conclusions Our study unravelled that LOXL1‐AS1/miR‐708‐5p/USF1 pathway contributed to the development of gastric cancer.

show abstract

Molecular Characterization, Expression Patterns, and Association Analysis with Carcass Traits of Porcine USF1 Gene

Cited by 12 publications

References 23 publications

RETRACTED: The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB

RETRACTED: The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB

RETRACTED: Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis

LncRNA LOXL1‐AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR‐708‐5p/USF1 pathway

Contact Info

Product

Resources

About