SP1-Mediated Upregulation of Long Noncoding RNA ZFAS1 Involved in Non-syndromic Cleft Lip and Palate via Inactivating WNT/β-Catenin Signaling Pathway

Chen, Shiyu; Jia, Zhong‐Lin; Cai, Ming; Ye, Mujie; Wu, Dandan; Wan, Teng; Zhang, Bowen; Wu, Peixuan; Xu, Yuexin; Guo, Yuntao; Tian, Chan; Ma, Duan; Ma, Jing

doi:10.3389/fcell.2021.662780

Cited by 11 publications

(9 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Meanwhile, miRNA‐binding site exists in some specific lncRNAs that control lncRNA and forward gene expression (Q. Liu et al, 2018). This might explain the SP1 differences in previous research, the predicted hsa‐miR‐1224‐3p in intermediate regulatory network might account for this opposite finding (Chen et al, 2021). Few studies have investigated hsa‐miR‐1224‐3p.…”

Section: Discussionmentioning

confidence: 76%

Long non‐coding RNAs MALAT1 and NEAT1 in non‐syndromic orofacial clefts

et al. 2022

View full text Add to dashboard Cite

Long non‐coding RNAs (lncRNAs) are thought to play important roles in non‐syndromic orofacial clefts (NSOFC). Clinical diagnosis was categorized as either non‐syndromic cleft lip with or without cleft palate (NSCL/P), or non‐syndromic cleft palate only (NSCPO). Tissues excised from the trimmed wound edge were reserved as experimental samples; adjacent normal control was used as a positive control, and tissue from healthy individuals was used as a blank control. Target lncRNAs in the collected tissues were identified using microarrays and quantitative reverse transcription PCR (RT‐qPCR). Immunohistochemical (IHC) staining and RT‐qPCR were used to verify the target mRNAs. Pathway, gene ontology (GO) enrichment, and TargetScan predictions were employed to construct competing endogenous RNA networks (ceRNA networks) and explore their potential functions. RNA‐Seq revealed 24 upregulated and 43 downregulated lncRNAs; MALAT1 and NEAT1 were screened and validated using RT‐qPCR. Common NSOFC risk factors were positively correlated with MALAT1 and NEAT1 expression. Bioinformatics predicted four ceRNA networks; GO enrichment focused on their potential functions. RT‐qPCR and IHC data were consistent with respect to expression levels of proteins and the mRNAs that encode them. As MALAT1 and NEAT1 are associated with the severity of NSOFC, they represent potential therapeutic targets and prognostic biomarkers.

show abstract

Section: Discussionmentioning

confidence: 76%

Long non‐coding RNAs MALAT1 and NEAT1 in non‐syndromic orofacial clefts

et al. 2022

View full text Add to dashboard Cite

show abstract

“…We next extended the analysis on binding transcription factors and found that risk-eSNPs were statistically significantly enriched in transcription factor binding sites, such as CHD1, GATA6, KDM4A, CTCF, TBP, E2F6, SP1, NANOG, YY1, and RAD21 ( Figure 2 C). Many of these transcription factors have been shown to be important in lip development or NSCL/P [ 22 , 23 , 24 , 25 , 26 ]. In addition, the eSNP-TF-eGene regulatory relationships for the top five TFs are listed in Table S5 .…”

Section: Resultsmentioning

confidence: 99%

Expression Quantitative Trait Locus Study of Non-Syndromic Cleft Lip with or without Cleft Palate GWAS Variants in Lip Tissues

Tian

Qiu

et al. 2022

Cells

View full text Add to dashboard Cite

Non-syndromic cleft lip with or without cleft palate (NSCL/P) is a complex disease with a strong genetic component. More than 40 loci have been identified to be associated with the risk of NSCL/P by genome-wide association studies (GWASs), but the majority of these variants are mapped to non-coding regions of the genome. Expression quantitative trait locus (eQTL) studies have increasingly been integrated with GWASs to identify target genes for these non-coding variants. In this study, we generated a unique, lip-specific eQTL dataset from 40 NSCL/P patients. A total of 5158 eQTL SNPs (eSNPs) -689 eQTL genes were identified after multiple corrections. Then, we integrated nominal eQTL SNPs with NSCL/P risk SNPs and identified 243 variants associated with the expression of 18 genes in lip tissues. Functional annotation analysis indicated that these risk eSNPs were significantly enriched in transcription regulation and chromatin open regions on the genome. These susceptible genes were enriched in cell fate determination, the pluripotency of stem cells, and Wnt signaling pathways. Finally, 8 of the 18 susceptible genes were differentially expressed in NSCL/P case-control studies. In summary, we have generated a unique lip-specific eQTL resource and identified multiple associations for NSCL/P risk loci, which should inform functional studies of NSCL/P biology.

show abstract

“…Likewise, our studies showed that LINC01608 was overexpressed in HCC and functioned as a ceRNA for miR‐875‐5p to promote HCC progression. Additionally, recent studies had demonstrated that some transcriptional factors, such as SP1 and MYBL2, could combine with the promoter of LncRNAs and regulate their expression 24,25 . YY1 is a transcriptional factor ubiquitously expressed in mammalian cells.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, recent studies had demonstrated that some transcriptional factors, such as SP1 and MYBL2, could combine with the promoter of LncRNAs and regulate their expression. 24,25 YY1 is a transcriptional factor ubiquitously expressed in mammalian cells. Previously published studies had indicated that YY1 could act as a transcriptional activator or a repressor and play important roles in several cancers.…”

Section: Discussionmentioning

confidence: 99%

LINC01608 activated by YY1 facilitate hepatocellular carcinoma progression by modulating the EGFR/ERK axis

Han

Liu

et al. 2022

Liver International

View full text Add to dashboard Cite

Background: Long non-coding RNAs (LncRNAs) have been demonstrated to associate with a variety of cancers. However, the mechanisms of LncRNAs in hepatocellular carcinoma (HCC) progression are still not fully clarified.Methods: LINC01608 expression level in HCC and adjacent normal tissues was detected by real-time-quantitively PCR (RT-qPCR) in clinical samples and in situ hybridization (ISH) in tissue microarray. Several functional assays were performed to determine the biological effects of LINC01608 in HCC cells in vitro, while subcutaneous xenograft models and lung metastasis models in nude mice and immunohistochemistry (IHC) results showed the role of LINC01608 in HCC progression in vivo.The combination of LINC01608 with miR-875-5p and target genes was elucidated by dual-luciferase report assays, RNA immunoprecipitation (RIP) assays and fluorescence in situ hybridization (FISH) assays. Finally, bioinformatics analysis and chromatin immunoprecipitation (CHIP) were performed to investigate the mechanism of Yin Yang-1 (YY1) regulating LINC01608 transcription.Results: LINC01608 was overexpressed in HCC tissues, and high LINC01608 expression predicted poor overall survival (OS) and disease-free survival (DFS) in HCC patients. LINC01608 could promote HCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and in vivo. Furthermore, we demonstrated that LINC01608 could sponge to miR-875-5p and activate the EGFR/ERK pathway. Moreover, we identified transcriptional factor YY1 could bind to the promoter of LINC01608 and induce its transcription. Conclusion:LINC01608 could serve as a promising prognostic biomarker of HCC. YY1-activated LINC01608 could promote HCC progression by associating with miR-875-5p to induce the EGFR/ERK signalling pathway. This discovery might provide therapeutic strategies for HCC.

show abstract

SP1-Mediated Upregulation of Long Noncoding RNA ZFAS1 Involved in Non-syndromic Cleft Lip and Palate via Inactivating WNT/β-Catenin Signaling Pathway

Cited by 11 publications

References 45 publications

Long non‐coding RNAs MALAT1 and NEAT1 in non‐syndromic orofacial clefts

Long non‐coding RNAs MALAT1 and NEAT1 in non‐syndromic orofacial clefts

Expression Quantitative Trait Locus Study of Non-Syndromic Cleft Lip with or without Cleft Palate GWAS Variants in Lip Tissues

LINC01608 activated by YY1 facilitate hepatocellular carcinoma progression by modulating the EGFR/ERK axis

Contact Info

Product

Resources

About