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Tytuł pozycji:

miRNA-34a-5p regulates progression of neuroblastoma via modulating the Wnt/β-catenin signaling pathway by targeting SOX4.

Tytuł:
miRNA-34a-5p regulates progression of neuroblastoma via modulating the Wnt/β-catenin signaling pathway by targeting SOX4.
Autorzy:
Wang Y; Qingdao Municipal Hospital Affiliated to Qingdao University.
Guan E; Qingdao Municipal Hospital Affiliated to Qingdao University.
Li D; Qingdao Women and Children's Hospital.
Sun L; The Affiliated Hospital of Qingdao University, No. 16 Jiangsu Road, Qingdao, P.R. China.
Źródło:
Medicine [Medicine (Baltimore)] 2021 May 21; Vol. 100 (20), pp. e25827.
Typ publikacji:
Journal Article; Observational Study
Język:
English
Imprint Name(s):
Original Publication: Hagerstown, Md : Lippincott Williams & Wilkins
MeSH Terms:
Gene Expression Regulation, Neoplastic*
MicroRNAs/*metabolism
Neuroblastoma/*genetics
SOXC Transcription Factors/*genetics
Wnt Signaling Pathway/*genetics
Apoptosis/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation ; Child ; Disease Progression ; Female ; Humans ; Male ; Neoplasm Invasiveness/genetics ; Neuroblastoma/pathology ; Neuroblastoma/surgery ; SOXC Transcription Factors/metabolism ; beta Catenin/metabolism
References:
Hoehner JC, Gestblom C, Hedborg F, Sandstedt B, Olsen L, Påhlman S. A developmental model of neuroblastoma: differentiating stroma-poor tumors’ progress along an extra-adrenal chromaffin lineage. Lab Invest 1996;75:659–75.
London WB, Castleberry RP, Matthay KK, et al. Evidence for an age cutoff greater than 365 days for neuroblastoma risk group stratification in the Children's Oncology Group. J Clin Oncol 2005;23:6459–65.
Carlsen NL. How frequent is spontaneous remission of neuroblastomas? Implications for screening. Br J Cancer 1990;61:441–6.
Cohn SL, Pearson AD, London WB, et al. The International Neuroblastoma Risk Group (INRG) classification system: an INRG Task Force report. J Clin Oncol 2009;27:289–97.
Elzomor H, Ahmed G, Elmenawi S, et al. Survival outcome of intermediate risk neuroblastoma at Children Cancer Hospital Egypt. J Egypt Natl Canc Inst 2018;30:21–6.
Tolbert VP, Matthay KK. Neuroblastoma: clinical and biological approach to risk stratification and treatment. Cell Tissue Res 2018;372:195–209.
Naidu S, Magee P, Garofalo M. MiRNA-based therapeutic intervention of cancer. J Hematol Oncol 2015;8:68.
Bartel DP. MicroRNAs: target recognition and regulatory functions. Cell 2009;136:215–33.
Wang K, Zhang S, Marzolf B, et al. Circulating microRNAs, potential biomarkers for drug-induced liver injury. Proc Natl Acad Sci U S A 2009;106:4402–7.
Arroyo JD, Chevillet JR, Kroh EM, et al. Argonaute2 complexes carry a population of circulating microRNAs independent of vesicles in human plasma. Proc Natl Acad Sci U S A 2011;108:5003–8.
Nonaka R, Nishimura J, Kagawa Y, et al. Circulating miR-199a-3p as a novel serum biomarker for colorectal cancer. Oncol Rep 2014;32:2354–8.
Mar-Aguilar F, Mendoza-Ramirez JA, Malagon-Santiago I, et al. Serum circulating microRNA profiling for identification of potential breast cancer biomarkers. Dis Markers 2013;34:163–9.
Si H, Sun X, Chen Y, et al. Circulating microRNA-92a and microRNA-21 as novel minimally invasive biomarkers for primary breast cancer. J Cancer Res Clin Oncol 2013;139:223–9.
Redova M, Poprach A, Nekvindova J, et al. Circulating miR-378 and miR-451 in serum are potential biomarkers for renal cell carcinoma. J Transl Med 2012;10:55.
Bommer GT, Gerin I, Feng Y, et al. p53-mediated activation of miRNA34 candidate tumor-suppressor genes. Curr Biol 2007;17:1298–307.
Chang TC, Wentzel EA, Kent OA, et al. Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Mol Cell 2007;26:745–52.
Vogt M, Munding J, Gruner M, et al. Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. Virchows Arch 2011;458:313–22.
Li N, Fu H, Tie Y, et al. miR-34a inhibits migration and invasion by down-regulation of c-Met expression in human hepatocellular carcinoma cells. Cancer Lett 2009;275:44–53.
Tryndyak VP, Ross SA, Beland FA, Pogribny IP. Down-regulation of the microRNAs miR-34a, miR-127, and miR-200b in rat liver during hepatocarcinogenesis induced by a methyl-deficient diet. Mol Carcinog 2009;48:479–87.
Feinberg-Gorenshtein G, Avigad S, Jeison M, et al. Reduced levels of miR-34a in neuroblastoma are not caused by mutations in the TP53 binding site. Genes Chromosomes Cancer 2009;48:539–43.
Wang X, Wang HK, McCoy JP, et al. Oncogenic HPV infection interrupts the expression of tumor-suppressive miR-34a through viral oncoprotein E6. RNA 2009;15:637–47.
Mraz M, Malinova K, Kotaskova J, et al. miR-34a, miR-29c and miR-17-5p are downregulated in CLL patients with TP53 abnormalities. Leukemia 2009;23:1159–63.
Welch C, Chen Y, Stallings RL. MicroRNA-34a functions as a potential tumor suppressor by inducing apoptosis in neuroblastoma cells. Oncogene 2007;26:5017–22.
Ding L, Zhao Y, Dang S, et al. Circular RNA circ-DONSON facilitates gastric cancer growth and invasion via NURF complex dependent activation of transcription factor SOX4. Mol Cancer 2019;18:45.
Moreno CS. SOX4: the unappreciated oncogene. Semin Cancer Biol 2020;67:57–64.
Zhang J, Xiao C, Feng Z, et al. SOX4 promotes the growth and metastasis of breast cancer. Cancer Cell Int 2020;20:468.
Bagati A, Kumar S, Jiang P, et al. Integrin αvβ6-TGFβ-SOX4 Pathway Drives Immune Evasion in Triple-Negative Breast Cancer. Cancer Cell 2021;39: 54-67.e59.
Guo Y, Xiao L, Sun L, Liu F. Wnt/beta-catenin signaling: a promising new target for fibrosis diseases. Physiol Res 2012;61:337–46.
Arend RC, Londoño-Joshi AI, Straughn JM Jr, Buchsbaum DJ. The Wnt/β-catenin pathway in ovarian cancer: a review. Gynecol Oncol 2013;131:772–9.
Krishnamurthy N, Kurzrock R. Targeting the Wnt/beta-catenin pathway in cancer: Update on effectors and inhibitors. Cancer Treat Rev 2018;62:50–60.
Buhagiar A, Ayers D. Chemoresistance, cancer stem cells, and miRNA influences: the case for neuroblastoma. Anal Cell Pathol (Amst) 2015;2015:150634.
Stigliani S, Morandi F, Persico L, et al. miRNA expression profile of bone marrow resident cells from children with neuroblastoma is not significantly different from that of healthy children. Oncotarget 2018;9:19014–25.
Chava S, Reynolds CP, Pathania AS, et al. miR-15a-5p, miR-15b-5p, and miR-16-5p inhibit tumor progression by directly targeting MYCN in neuroblastoma. Mol Oncol 2020;14:180–96.
Neviani P, Wise PM, Murtadha M, et al. Natural killer-derived exosomal mir-186 inhibits neuroblastoma growth and immune escape mechanisms. Cancer Res 2019;79:1151–64.
Schmittgen TD. Exosomal miRNA Cargo as Mediator of Immune Escape Mechanisms in Neuroblastoma. Cancer Res 2019;79:1293–4.
Tao T, Shi H, Mariani L, et al. LIN28B regulates transcription and potentiates MYCN-induced neuroblastoma through binding to ZNF143 at target gene promotors. Proc Natl Acad Sci U S A 2020;117:16516–26.
Li XY, Wen JY, Jia CC, et al. MicroRNA-34a-5p enhances sensitivity to chemotherapy by targeting AXL in hepatocellular carcinoma MHCC-97L cells. Oncol Lett 2015;10:2691–8.
Ma Y, Huang YX, Chen YY. miRNA34a5p downregulation of VEGFA in endometrial stem cells contributes to the pathogenesis of endometriosis. Mol Med Rep 2017;16:8259–64.
Tian Z, Yang G, Jiang P, Zhang L, Wang J, Sun S. Long non-coding RNA Sox4 promotes proliferation and migration by activating Wnt/β-catenin signaling pathway in osteosarcoma. Pharmazie 2017;72:537–42.
Wang C, Zi H, Wang Y, Li B, Ge Z, Ren X. LncRNA CASC15 promotes tumour progression through SOX4/Wnt/β-catenin signalling pathway in hepatocellular carcinoma. Artif Cells Nanomed Biotechnol 2020;48:763–9.
Zhao G, Yin Y. Zhao B. miR-140-5p is negatively correlated with proliferation, invasion, and tumorigenesis in malignant melanoma by targeting SOX4 via the Wnt/β-catenin and NF-κB cascades. J Cell Physiol 2020;235:2161–70.
Substance Nomenclature:
0 (CTNNB1 protein, human)
0 (MIRN34 microRNA, human)
0 (MicroRNAs)
0 (SOX4 protein, human)
0 (SOXC Transcription Factors)
0 (beta Catenin)
Entry Date(s):
Date Created: 20210520 Date Completed: 20210527 Latest Revision: 20230103
Update Code:
20240104
PubMed Central ID:
PMC8137035
DOI:
10.1097/MD.0000000000025827
PMID:
34011046
Czasopismo naukowe
Abstract: Neuroblastoma is an embryonal tumor of the autonomic nervous system with poor prognosis in children. In present study, we demonstrated the relationship of miRNA-34a-5p in the regulating of the Wnt/β-catenin signaling pathway by targeting SRY-related HMG-box (SOX4)Reverse transcription-quantitative PCR was used to detect the expression levels of miRNA-34a-5p and SoX4. Western blotting was performed to assess the protein expression levels of SoX4, Wnt, MMP9, Bax, and Bcl-2. The proliferation, apoptosis, migration and invasion of neuroblastoma cells were determined using MTT, flow cytometry and Transwell assays.In this study, we sought to investigate the role of miRNA-34a-5p on neuroblastoma and the possible molecular mechanism. We had performed in-vitro and in-vivo experiments to evaluate the effects of miRNA-34a-5p on neuroblastoma cell proliferation and invasion by altering its expression level via cell transfection. On the basis of our study, miRNA-34a-5p showed decreased expression levels in neuroblastoma. Subsequently, we manipulated miRNA-34a-5p expression through cell transfection and observed abnormal expression of β-catenin as well as the downstream targets of the Wnt/β-catenin pathway in neuroblastoma cells. With all these evidences, we determined that miRNA-34a-5p regulated Wnt/β-catenin pathway by targeting SOX4.In conclusion, our study demonstrates that miRNA-34a-5p can inhibit the over-activation of the Wnt/β-catenin signaling pathway via targeting SOX4 and further regulate proliferation, invasion of neuroblastoma cells.
Competing Interests: The authors have no conflicts of interest to disclose.
(Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

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