Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.
ADVANCED SEARCH
Log in
Top
Tumor Biology
Published in: Tumor Biology 6/2016

01-06-2016 | Original Article

RETRACTED ARTICLE: miR-494 suppresses tumor growth of epithelial ovarian carcinoma by targeting IGF1R

Authors: Na Li, Xiaosu Zhao, Lufei Wang, Shi Zhang, Manhua Cui, Jin He

Published in: Tumor Biology | Issue 6/2016

Login to get access

Abstract

A growing body of evidence suggests that microRNA-494 (miR-494) could act as tumor-suppressive or oncogenic microRNAs (miRNAs) in different types of tumors. However, the biological roles and underlying mechanisms of miR-494 remain unknown in human epithelial ovarian carcinoma (EOC). Therefore, the aims of this study were to investigate the miR-494 expression and the significance of its clinical diagnosis in patients suffering EOC and to analyze its role and underlying molecular mechanism on the carcinogenesis of EOC. Here, we found that miR-494 was significantly decreased in EOC cell lines and tissues and its expression was negatively correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, high pathological grade, and lymph node metastasis (all P < 0.01). Functional studies showed that overexpression of miR-494 in EOC cells could remarkably inhibit proliferation, colony formation, migration, and invasion and induce cell apoptosis, G0/G1 phase arrest. An in vivo analysis revealed that the overexpression of miR-494 suppressed tumor growth in a nude mouse xenograft model system. Bioinformatic assay and dual-luciferase assay confirmed that insulin-like growth factor 1 receptor (IGF1R) was as a direct target of miR-494 in EOC cells. Western blot assay showed that overexpression of miR-494 inhibited IGF1R expression and its downstream signal protein expression. In addition, downregulation of IGF1R has similar effects with miR-494 overexpression on EOC cells and overexpression of IGF1R effectively rescued the inhibition of overexpressed miR-494 in EOC cells. These data suggested that miR-494 functions as a tumor suppressor in EOC by targeting IGF1R.
Literature
1.
2.
3.
Legge F, Ferrandina G, Salutari V, Scambia G. Biological characterization of ovarian cancer: prognostic and therapeutic implications. Ann Oncol. 2005;16:95–101.CrossRef
4.
Coleman RL, Monk BJ, Sood AK, Herzog TJ. Latest research and treatment of advanced-stage epithelial ovarian cancer. Nat Rev Clin Oncol. 2013;10:211–24.CrossRefPubMedPubMedCentral
5.
Miska EA. How microRNAs control cell division, differentiation and death. Curr Opin Genet Dev. 2005;15:563.CrossRefPubMed
6.
7.
Brennecke J, Hipfner DR, Stark A, Russell RB, Cohen SM. Bantam encodes a developmentally regulated microRNA that controls cell proliferation and regulates the proapoptotic gene hid in Drosophila. Cell. 2003;113:25–36.CrossRefPubMed
8.
9.
Seton-Rogers S. Tumour suppressors: Hippo promotes microRNA processing. Nat Rev Cancer. 2014;14:216–7.PubMed
10.
Shenouda SK, Alahari SK. MicroRNA function in cancer: oncogene or a tumor suppressor? Cancer Metastasis Rev. 2009;28:369–78.CrossRefPubMed
11.
Zhang X, Han C, He J: Research progress of oncogene and tumor suppressor gene in bladder cancer. Panminerva Med. 2015 (in press).
12.
Diakos C, Zhong S, Xiao Y, Zhou M, Vasconcelos GM, Krapf G, et al. TEL-AML1 regulation of survivin and apoptosis via miRNA-494 and miRNA-320a. Blood. 2010;116:4885–93.CrossRefPubMedPubMedCentral
13.
Duan H, Jiang Y, Zhang H, Wu Y. MiR-320 and miR-494 affect cell cycles of primary murine bronchial epithelial cells exposed to benzo[a]pyrene. Toxicol In Vitro. 2010;24:928–35.CrossRefPubMed
14.
Zhao JJ, Yang J, Lin J, Yao N, Zhu Y, Zheng J, et al. Identification of miRNAs associated with tumorigenesis of retinoblastoma by miRNA microarray analysis. Childs Nerv Syst. 2009;25:13–20.CrossRefPubMed
15.
Liu K, Liu S, Zhang W, Jia B, Tan L, Jin Z, et al. miR-494 promotes cell proliferation, migration and invasion, and increased sorafenib resistance in hepatocellular carcinoma by targeting PTEN. Oncol Rep. 2015;34:1003–10.CrossRefPubMed
16.
Lim L, Balakrishnan A, Huskey N, Jones KD, Jodari M, Ng R, et al. MicroRNA-494 within an oncogenic microRNA megacluster regulates G1/S transition in liver tumorigenesis through suppression of mutated in colorectal cancer. Hepatology. 2014;59:202–15.CrossRefPubMed
17.
Liu Y, Li X, Zhu S, Zhang JG, Yang M, Qin Q, et al. Ectopic expression of miR-494 inhibited the proliferation, invasion and chemoresistance of pancreatic cancer by regulating SIRT1 and c-Myc. Gene Ther. 2015;22:729–38.CrossRefPubMed
18.
Shen PF, Chen XQ, Liao YC, Chen N, Zhou Q, Wei Q, et al. MicroRNA-494-3p targets CXCR4 to suppress the proliferation, invasion, and migration of prostate cancer. Prostate. 2014;74:756–67.CrossRefPubMed
19.
Romano G, Acunzo M, Garofalo M, Di Leva G, Cascione L, Zanca C, et al. MiR-494 is regulated by ERK1/2 and modulates trail-induced apoptosis in non-small-cell lung cancer through BIM down-regulation. Proc Natl Acad Sci U S A. 2012;109:16570–5.CrossRefPubMedPubMedCentral
20.
Kim WK, Park M, Kim YK, Tae YK, Yang HK, Lee JM, et al. MicroRNA-494 downregulates kit and inhibits gastrointestinal stromal tumor cell proliferation. Clin Cancer Res. 2011;17:7584–94.CrossRefPubMed
21.
Yamanaka S, Campbell NR, An F, Kuo SC, Potter JJ, Mezey E, et al. Coordinated effects of microRNA-494 induce G2/M arrest in human cholangiocarcinoma. Cell Cycle. 2012;11:2729–38.CrossRefPubMedPubMedCentral
22.
Kim YW, Kim EY, Jeon D, Liu JL, Kim HS, Choi JW, et al. Differential microRNA expression signatures and cell type-specific association with taxol resistance in ovarian cancer cells. Drug Des Devel Ther. 2014;8:293–314.PubMedPubMedCentral
23.
Sanabria-Figueroa E, Donnelly SM, Foy KC, Buss MC, Castellino RC, Paplomata E, et al. Insulin-like growth factor-1 receptor signaling increases the invasive potential of human epidermal growth factor receptor 2-overexpressing breast cancer cells via Src-focal adhesion kinase and forkhead box protein M1. Mol Pharmacol. 2015;87:150–61.CrossRefPubMedPubMedCentral
24.
King SM, Modi DA, Eddie SL, Burdette JE. Insulin and insulin-like growth factor signaling increases proliferation and hyperplasia of the ovarian surface epithelium and decreases follicular integrity through upregulation of the PI3-kinase pathway. J Ovarian Res. 2013;6:12.CrossRefPubMedPubMedCentral
25.
Osaki LH, Gama P. MAPKs and signal transduction in the control of gastrointestinal epithelial cell proliferation and differentiation. Int J Mol Sci. 2013;14:10143–61.CrossRefPubMedPubMedCentral
26.
Cao Z, Liu LZ, Dixon DA, Zheng JZ, Chandran B, Jiang BH. Insulin-like growth factor-I induces cyclooxygenase-2 expression via PI3K, MAPK and PKC signaling pathways in human ovarian cancer cells. Cell Signal. 2007;19:1542–53.CrossRefPubMedPubMedCentral
27.
Gest C, Mirshahi P, Li H, Pritchard LL, Joimel U, Blot E, et al. Ovarian cancer: Stat3, RhoA and IGF-IR as therapeutic targets. Cancer Lett. 2012;317:207–17.CrossRefPubMed
28.
Gotlieb WH, Bruchim I, Gu J, Shi Y, Camirand A, Blouin MJ, et al. Insulin-like growth factor receptor I targeting in epithelial ovarian cancer. Gynecol Oncol. 2006;100:389–96.CrossRefPubMed
29.
Coppola D, Saunders B, Fu L, Mao W, Nicosia SV. The insulin-like growth factor 1 receptor induces transformation and tumorigenicity of ovarian mesothelial cells and down-regulates their Fas-receptor expression. Cancer Res. 1999;59:3264–70.PubMed
30.
Xue M, Cao X, Zhong Y, Kuang D, Liu X, Zhao Z, et al. Insulin-like growth factor-1 receptor (IGF1R) kinase inhibitors in cancer therapy: advances and perspectives. Curr Pharm Des. 2012;18:2901–13.CrossRefPubMed
Metadata
Title
RETRACTED ARTICLE: miR-494 suppresses tumor growth of epithelial ovarian carcinoma by targeting IGF1R
Authors
Na Li
Xiaosu Zhao
Lufei Wang
Shi Zhang
Manhua Cui
Jin He
Publication date
01-06-2016
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 6/2016
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-4603-8

Other articles of this Issue 6/2016

Tumor Biology 6/2016 Go to the issue

Original Article

Downregulation of SATB1 increases the invasiveness of Jurkat cell via activation of the WNT/β-catenin signaling pathway in vitro

Original Article

The search for optimal cutoff points for apoptosis and proliferation rate in prognostification of early stage breast cancer patients treated with anthracyclines in adjuvant settings

Original Article

Expression of cancer-associated fibroblast-related proteins in thyroid papillary carcinoma

Original Article

Identification of serum miRNAs by nano-quantum dots microarray as diagnostic biomarkers for early detection of non-small cell lung cancer

Original Article

Association of ABCB1 and ABCG2 single nucleotide polymorphisms with clinical findings and response to chemotherapy treatments in Kurdish patients with breast cancer

Original Article

CUL4A expression in pediatric osteosarcoma tissues and its effect on cell growth in osteosarcoma cells
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits