Downregulation of miR-152 contributes to DNMT1-mediated silencing of SOCS3/SHP-1 in non-Hodgkin lymphoma

Wang, Qing-Ming; Lian, Guang-Yu; Song, Yuan; Peng, Zhi-Da; Xu, Shengyuan; Gong, Yi

doi:10.1038/s41417-018-0057-7

Cited by 22 publications

(12 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oxidative Medicine and Cellular Longevity may be responsible for aggressive tumor growth in DNMT3b-positive ESCC cells [24]. Previous studies have validated that DNMT1 negatively regulates SOCS3 expression in several types of cancer cells [25][26][27]. In the present study, we found that the demethylation agent 5-aza restored SOCS3 mRNA expression to different degrees.…”

Section: Discussionsupporting

confidence: 69%

THAP9‐AS1 Promotes Tumorigenesis and Reduces ROS Generation through the JAK2/STAT3 Signaling Pathway by Increasing SOCS3 Promoter Methylation in Osteosarcoma

Yang

Wang

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Increasing studies have demonstrated that dysfunction of long noncoding RNAs (lncRNAs) plays critical roles in the development of human cancers. THAP9-AS1 has been reported to be dysregulated and associated with tumor progression in some cancers. However, the function and mechanism of THAP9-AS1 in osteosarcoma (OS) remain unclear. In the present study, we found that the expression of THAP9-AS1 was significantly upregulated in OS tissues and associated with the advanced stage of tumors and poor prognosis of patients. Blast comparison results showed that the SOCS3 promoter region and THAP9-AS1 had base complementary pairing binding sites. The interactions between THAP9-AS1, DNA methyltransferases (DNMTs), and SOCS3 were assessed by RIP and ChIP assays. The results of methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP) validated that THAP9-AS1 enhanced the methylation level of the SOCS3 promoter. The mRNA levels of SOCS3 in OS cells could be reversed by the demethylation agent 5-aza-2 ′ -deoxycytidine. The mRNA expression of SOCS3 was downregulated in OS tissues and negatively correlated with THAP9-AS1 expression in tumors. Moreover, the western blot and immunofluorescence (IF) assay data showed that THAP9-AS1 activated the JAK2/STAT3 signaling pathway by upregulating p-JAK2 and p-STAT3 and the nuclear translocation of p-STAT3. Functionally, ectopic expression of THAP9-AS1 promoted cell proliferation, migration, and invasion and inhibited apoptosis, and this phenomenon could be reversed by SOCS3. Introduction of the JAK/STAT inhibitor AG490 partially abolished the stimulative effect of THAP9-AS1 on cellular processes. In addition, THAP9-AS1 decreased oxidative stress by reducing reactive oxygen species (ROS) and enhancing the mitochondrial membrane potential of OS cells via the SOCS3/JAK2/STAT3 pathway. Stable overexpression of THAP9-AS1 contributed to tumor growth and metastasis in vivo. In total, our findings suggested that upregulation of THAP9-AS1 might recruit DNMTs to epigenetically inhibit SOCS3, thereby activating the JAK2/STAT3 signaling pathway and oncogenesis of OS. These results provide novel insights for the understanding of OS progression.

show abstract

Section: Discussionsupporting

confidence: 69%

THAP9‐AS1 Promotes Tumorigenesis and Reduces ROS Generation through the JAK2/STAT3 Signaling Pathway by Increasing SOCS3 Promoter Methylation in Osteosarcoma

Yang

Wang

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…MYCNOS promotes the invasion and metastasis of neuroblastoma and rhabdomyosarcoma by regulating MYCN protein (24,25) and may participate in the development of WT (26). miR-152 targeting DNMT1 inhibits the development of endometrial cancer (27), glioblastoma (28), and lymphomas (29). miR-181a mediates the Wnt/b-catenin pathway to accelerate the progression of colorectal cancer (30), oral squamous cell carcinoma (31), and acute lymphoblastic leukemia (32).…”

Section: Discussionmentioning

confidence: 99%

A Survival-Related Competitive Endogenous RNA Network of Prognostic lncRNAs, miRNAs, and mRNAs in Wilms Tumor

et al. 2021

View full text Add to dashboard Cite

Wilms tumor (WT) commonly occurs in infants and children. We evaluated clinical factors and the expression of multiple RNAs in WT samples in the TARGET database. Eight long non-coding RNAs (lncRNAs; AC079310.1, MYCNOS, LINC00271, AL445228.3, Z84485.1, AC091180.5, AP002518.2, and AC007879.3), two microRNAs (miRNAs; hsa-mir-152 andhsa-mir-181a), and nine messenger RNAs (mRNAs; TCTEX1D4, RNF133, VRK1, CCNE1, HEY1, C10orf71, SPRY1, SPAG11A, and MAGEB18) were screened from differentially expressed RNAs and used to construct predictive survival models. These models showed good prognostic ability and were highly correlated with tumor stage and histological classification. Additionally, survival-related ceRNA network was constructed using 35 RNAs (15 lncRNAs, eight miRNAs, and 12 mRNAs). KEGG pathway analysis suggested the “Wnt signaling pathway” and “Cellular senescence” as the main pathways. In conclusion, we established a multinomial predictive survival model and a survival-related ceRNA network, which provide new potential biomarkers that may improve the prognosis and treatment of WT patients.

show abstract

“…The dual luciferase reporter assay was carried out as previously described [ 39 – 42 ]. Briefly, the wild-type and mutant circRNA_30032, and wild-type and mutant 3’UTR’s of HBEGF and KRAS were cloned into the pmir GLO dual-luciferase target expression vector, and co-transfected with miR-96-5p mimics into the BUMPT cells.…”

Section: Methodsmentioning

confidence: 99%

CircRNA_30032 promotes renal fibrosis in UUO model mice via miRNA-96-5p/HBEGF/KRAS axis

Lee

et al. 2021

Aging

View full text Add to dashboard Cite

In this study, we investigated the role of circular RNA_30032 (circRNA_30032) in renal fibrosis and the underlying mechanisms. The study was carried out using TGF-β1-induced BUMPT cells and unilateral ureteral obstruction (UUO)-induced mice, respectively, as in vitro and in vivo models. CircRNA_30032 expression was significantly increased by 9.15- and 16.6-fold on days 3 and 7, respectively, in the renal tissues of UUO model mice. In TGF-β1-treated BUMPT cells, circRNA_30032 expression was induced by activation of the p38 mitogen-activated protein kinase signaling pathway. Quantitative real-time PCR, western blotting and dual luciferase reporter assays showed that circRNA_30032 mediated TGF-β1-induced and UUO-induced renal fibrosis by sponging miR-96-5p and increasing the expression of profibrotic proteins, including HBEGF, KRAS, collagen I, collagen III and fibronectin. CircRNA_30032 silencing significantly reduced renal fibrosis in UUO model mice by increasing miR-96-5p levels and decreasing levels of HBEGF and KRAS. These results demonstrate that circRNA_30032 promotes renal fibrosis via the miR-96-5p/HBEGF/KRAS axis and suggest that circRNA_30032 is a potential therapeutic target for treatment of renal fibrosis.

show abstract

Downregulation of miR-152 contributes to DNMT1-mediated silencing of SOCS3/SHP-1 in non-Hodgkin lymphoma

Cited by 22 publications

References 46 publications

THAP9‐AS1 Promotes Tumorigenesis and Reduces ROS Generation through the JAK2/STAT3 Signaling Pathway by Increasing SOCS3 Promoter Methylation in Osteosarcoma

THAP9‐AS1 Promotes Tumorigenesis and Reduces ROS Generation through the JAK2/STAT3 Signaling Pathway by Increasing SOCS3 Promoter Methylation in Osteosarcoma

A Survival-Related Competitive Endogenous RNA Network of Prognostic lncRNAs, miRNAs, and mRNAs in Wilms Tumor

CircRNA_30032 promotes renal fibrosis in UUO model mice via miRNA-96-5p/HBEGF/KRAS axis

Contact Info

Product

Resources

About