Regulatory Fluctuation of WNT16 Gene Expression Is Associated with Human Gastric Adenocarcinoma

Norollahi, Seyedeh Elham; Alipour, Majid; Rashidy-Pour, Ali; Samadani, Ali Akbar; Larijani, Laleh Vahedi

doi:10.1007/s12029-017-0022-y

Cited by 19 publications

(7 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, Wnt-16 has been shown to activate human keratinocyte proliferation (30). Furthermore, compared normal tissues, the expression of Wnt-16 was upregulated in tumoral tissues, indicating that Wnt-16 may be associated with the progression of gastric cancer (31). Therefore, the abnormal expression of Wnt-16 we found suggests Wnt-related signaling may be involved in the pathogenesis of SLE.…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0000479 as a Novel Diagnostic Biomarker of Systemic Lupus Erythematosus

Guo

Wang

et al. 2019

Front. Immunol.

View full text Add to dashboard Cite

Background: Accumulating evidence suggests that differentially expressed non-coding circular RNAs (circRNAs) play critical roles in the progress of autoimmune diseases. However, the role of circRNAs in systemic lupus erythematosus (SLE) remains unclear.Methods: We initially used next-generation sequencing (NGS) to comprehensively analyze circRNA expression profiles in peripheral blood mononuclear cells (PBMCs) from 10 SLE patients, stratified by their disease activity characteristics (stable or active SLE), and 10 healthy controls (HCs). Candidate circRNAs identified were first validated by quantitative reverse-transcription (qRT)-PCR in PBMC samples from a training-phase cohort of five SLE patients and five HCs. The significantly dysregulated circRNAs were then confirmed by qRT-PCR in a validation cohort of 23 SLE patients and 21 HCs, and in an external validation cohort with 64 SLE patients, 58 HCs, and 50 patients with rheumatoid arthritis (RA). In addition, we conducted bioinformatics analysis and western blotting investigating the relationships between the candidate circRNAs and SLE progression.Results: Multilayer integrative analysis of circRNA regulation showed that 84 circRNAs were upregulated and 30 were downregulated in patients with SLE compared with HCs. We then analyzed the intersection of these differentially expressed circRNAs in an SLE-stable cohort, an SLE-active cohort, and HCs. This enabled us to narrow down dysregulated circRNAs to 15 upregulated circRNAs. Only hsa_circ_0000479 was significantly upregulated in PBMCs of patients with SLE compared with HCs (P < 0.05). Furthermore, the diagnostic potential of hsa_circ_0000479 expression to distinguish SLE patients from HCs and RA patients was also significantly increased in the validation-phase and external-validation-phase cohorts (P < 0.05). When distinguishing SLE patients from HCs, the diagnostic specificities of hsa_circ_0000479 were 0.619 and 1.0 in two validation cohorts, respectively (AUCs = 0.731 and 0.730, respectively). It was also significantly increased in either stable SLE patients or active SLE patients compared with HCs in these two cohorts (P < 0.05). We also used bioinformatics analysis to show that hsa_circ_0000479 regulates SLE progression by modulating metabolic pathways and the Wnt signaling pathway. Western blotting revealed that the expression of Wnt-16 protein was significantly decreased in SLE.Conclusion: Our results suggest that hsa_circ_0000479 has potential as a novel biomarker for the diagnosis of SLE.

show abstract

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0000479 as a Novel Diagnostic Biomarker of Systemic Lupus Erythematosus

Guo

Wang

et al. 2019

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…It is now accepted that Wnt16 contributes to skeletal development and postnatal bone homeostasis via activating the canonical and the non-canonical Wnt signaling cascades (135). Wnt16 is overexpressed in gastric adenocarcinoma, leiomyoma, and head and neck squamous cell carcinoma tissues (136,137). Upregulation of Wnt16 induced by estrogen and progesterone treatment in uterine leiomyoma stem cells could promote the growth of uterine leiomyomas through activating the canonical Wnt pathway in a paracrine manner (138), and the enhanced β-catenin activities initiated by Wnt16 in prostate cancer cells could promote the malignant phenotypes and chemoresistance through preventing cell death (139).…”

Section: Wnt16mentioning

confidence: 99%

Emerging Roles of Wnt Ligands in Human Colorectal Cancer

et al. 2020

View full text Add to dashboard Cite

Colorectal cancer (CRC) is the fourth leading cause of cancer death worldwide, and constitutive activation of the Wnt signaling pathway is universal in most CRC cases. Wnt ligands (Wnts) are secreted glycoproteins and fundamentally essential for the transduction of Wnt signaling pathway. However, the 19 members of Wnts in humans imply a daunting complexity of Wnt signaling and biological effects, and our understanding of their roles in CRC tumorigenesis is still quite rudimentary. This review will give an overview of the structural characteristics and maturation process of Wnts. The expression pattern of all human Wnts in CRC tissues, including Wnt1, Wnt2,

show abstract

“…Epigenetics consist of DNA methylation, histone modification, histone acetylation, histone phosphorylation and also RNA remodeling which DNA methylation is the most important element [6][7][8][9][10][11][12]. Meanwhile, alongside with the investigation of epigenetics fluctuation in GI cancers, gene expression study must be added in order to have a better comparison and result [13][14][15][16][17][18][19][20].…”

Section: Epigenetic and Cancermentioning

confidence: 99%

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

Babaei¹,

Khaksar²,

Zeinali³

et al. 2019

BioMedicine

Self Cite

View full text Add to dashboard Cite

Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.

show abstract

Regulatory Fluctuation of WNT16 Gene Expression Is Associated with Human Gastric Adenocarcinoma

Abstract: Conclusively, the upregulation of WNTt16 gene expression in tumoral tissues was impressive and the P value was 0.005 and the SE range was 0.064-142.154.

Cited by 19 publications

References 18 publications

Hsa_circ_0000479 as a Novel Diagnostic Biomarker of Systemic Lupus Erythematosus

Hsa_circ_0000479 as a Novel Diagnostic Biomarker of Systemic Lupus Erythematosus

Emerging Roles of Wnt Ligands in Human Colorectal Cancer

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

Contact Info

Product

Resources

About