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
Cancer Cell International
Published in: Cancer Cell International 1/2017

Open Access 01-12-2017 | Primary research

miR-324-3p suppresses migration and invasion by targeting WNT2B in nasopharyngeal carcinoma

Authors: Chao Liu, Guo Li, Nianting Yang, Zhongwu Su, Shuiting Zhang, Tengbo Deng, Shuling Ren, Shanhong Lu, Yongquan Tian, Yong Liu, Yuanzheng Qiu

Published in: Cancer Cell International | Issue 1/2017

Login to get access

Abstract

Background

Nasopharyngeal carcinoma (NPC) is a malignant epithelial carcinoma of the head and neck with strong ability of invasion and metastasis. Our previous study indicated that miR-324-3p, as a tumor-suppressive factor, could regulate radioresistance of NPC cells by targeting WNT2B. The purpose of this study is to investigate the role of miR-324-3p on migration and invasion in NPC cells.

Methods

Quantitative real time PCR was applied to measure the expression level of miR-324-3p and WNT2B mRNA in both cells and tissues, and the expression level of WNT2B protein was determined by western blotting. The capacity of migration and invasion were tested by using wound healing and transwell invasion assay.

Results

Ectopic expression of miR-324-3p or silencing its target gene WNT2B could dramatically suppress migration and invasion capacity of NPC cells. Meanwhile, the alterations of miR-324-3p in NPC cells could influence the expression level of the biomarkers of epithelial-mesenchymal transition (EMT), including E-cadherin and Vimentin. Moreover, the expression of miR-324-3p was obviously downregulated and WNT2B was significantly upregulated in NPC tissues. The expression levels of miR-324-3p and WNT2B were closely correlated with T stage, clinic stage and cervical lymph node metastasis of NPC (P < 0.05).

Conclusion

miR-324-3p could suppress the migration and invasion of NPC by targeting WNT2B and the miR-324-3p/WNT2B pathway possibly provide new potential therapeutic clues for NPC.
Appendix
Available only for authorised users
Literature
1.
Torre LA, Bray F, Siegel RL, Ferlay J, Lortet-Tieulent J, Jemal A. Global cancer statistics 2012. CA Cancer J Clin. 2015;65:87–108.CrossRefPubMed
2.
Razak AR, Siu LL, Liu FF, Ito E, O’Sullivan B, Chan K. Nasopharyngeal carcinoma: the next challenges. Eur J Cancer. 2010;46:1967–78.CrossRefPubMed
3.
Bensouda Y, Kaikani W, Ahbeddou N, Rahhali R, Jabri M, Mrabti H, Boussen H, Errihani H. Treatment for metastatic nasopharyngeal carcinoma. Eur Ann Otorhinolaryngol Head Neck Dis. 2011;128:79–85.CrossRefPubMed
4.
5.
Lytle JR, Yario TA, Steitz JA. Target mRNAs are repressed as efficiently by microRNA-binding sites in the 5′ UTR as in the 3′ UTR. Proc Natl Acad Sci USA. 2007;104:9667–72.CrossRefPubMedPubMedCentral
6.
Gu W, Wang X, Zhai C, Zhou T, Xie X. Biological basis of miRNA action when their targets are located in human protein coding region. PLoS ONE. 2013;8:e63403.CrossRefPubMedPubMedCentral
7.
8.
Ou H, Li Y, Kang M. Activation of miR-21 by STAT3 induces proliferation and suppresses apoptosis in nasopharyngeal carcinoma by targeting PTEN gene. PLoS ONE. 2014;9:e109929.CrossRefPubMedPubMedCentral
9.
Qu JQ, Yi HM, Ye X, Li LN, Zhu JF, Xiao T, Yuan L, Li JY, Wang YY, Feng J, He QY, Lu SS, Yi H, Xiao ZQ. MiR-23a sensitizes nasopharyngeal carcinoma to irradiation by targeting IL-8/Stat3 pathway. Oncotarget. 2015;6:28341–56.CrossRefPubMed
10.
Peng X, Cao P, Li J, He D, Han S, Zhou J, Tan G, Li W, Yu F, Yu J, Li Z, Cao K. MiR-1204 sensitizes nasopharyngeal carcinoma cells to paclitaxel both in vitro and in vivo. Cancer Biol Ther. 2015;16:261–7.CrossRefPubMedPubMedCentral
11.
Huang H, Sun P, Lei Z, Li M, Wang Y, Zhang HT, Liu J. MiR-145 inhibits invasion and metastasis by directly targeting Smad3 in nasopharyngeal cancer. Tumour Biol. 2015;36:4123–31.CrossRefPubMed
12.
Fang Y, Zhu X, Wang J, Li N, Li D, Sakib N, Sha Z, Song W. MiR-744 functions as a proto-oncogene in nasopharyngeal carcinoma progression and metastasis via transcriptional control of ARHGAP5. Oncotarget. 2015;6:13164–75.CrossRefPubMedPubMedCentral
13.
Li G, Liu Y, Su Z, Ren S, Zhu G, Tian Y, Qiu Y. MicroRNA-324-3p regulates nasopharyngeal carcinoma radioresistance by directly targeting WNT2B. Eur J Cancer. 2013;49:2596–607.CrossRefPubMed
14.
Li G, Wang Y, Liu Y, Su Z, Liu C, Ren S, Deng T, Huang D, Tian Y, Qiu Y. MiR-185-3p regulates nasopharyngeal carcinoma radioresistance by targeting WNT2B in vitro. Cancer Sci. 2014;105:1560–8.CrossRefPubMedPubMedCentral
15.
Kim J, Krichevsky A, Grad Y, Hayes GD, Kosik KS, Church GM, Ruvkun G. Identification of many microRNAs that copurify with polyribosomes in mammalian neurons. Proc Natl Acad Sci USA. 2004;101:360–5.CrossRefPubMed
16.
Hu Z, Dong J, Wang LE, Ma H, Liu J, Zhao Y, Tang J, Chen X, Dai J, Wei Q, Zhang C, Shen H. Serum microRNA profiling and breast cancer risk: the use of miR-484/191 as endogenous controls. Carcinogenesis. 2012;33:828–34.CrossRefPubMed
17.
Wen Y, Han J, Chen J, Dong J, Xia Y, Liu J, Jiang Y, Dai J, Lu J, Jin G, Han J, Wei Q, Shen H, Sun B, Hu Z. Plasma miRNAs as early biomarkers for detecting hepatocellular carcinoma. Int J Cancer. 2015;137:1679–90.CrossRefPubMed
18.
Namkung J, Kwon W, Choi Y, Yi SG, Han S, Kang MJ, Kim SW, Park T, Jang JY. Molecular subtypes of pancreatic cancer based on miRNA expression profiles have independent prognostic value. J Gastroenterol Hepatol. 2016;31:1160–7.CrossRefPubMed
19.
Macconi D, Tomasoni S, Romagnani P, Trionfini P, Sangalli F, Mazzinghi B, Rizzo P, Lazzeri E, Abbate M, Remuzzi G, Benigni A. MicroRNA-324-3p promotes renal fibrosis and is a target of ACE inhibition. J Am Soc Nephrol. 2012;23:1496–505.CrossRefPubMedPubMedCentral
20.
21.
Xu J, Ai Q, Cao H, Liu Q. MiR-185-3p and miR-324-3p predict radiosensitivity of nasopharyngeal carcinoma and modulate cancer cell growth and apoptosis by targeting SMAD7. Med Sci Monit. 2015;21:2828–36.CrossRefPubMedPubMedCentral
22.
Katoh M. Differential regulation of WNT2 and WNT2B expression in human cancer. Int J Mol Med. 2001;8:657–60.PubMed
23.
Li SJ, Yang XN, Qian HY. Antitumor effects of WNT2B silencing in GLUT1 overexpressing cisplatin resistant head and neck squamous cell carcinoma. Am J Cancer Res. 2015;5:300–8.PubMed
24.
Kobayashi M, Huang CL, Sonobe M, Kikuchi R, Ishikawa M, Kitamura J, Miyahara R, Menju T, Iwakiri S, Itoi K, Yasumizu R, Date H. Intratumoral Wnt2B expression affects tumor proliferation and survival in malignant pleural mesothelioma patients. Exp Ther Med. 2012;3:952–8.PubMedPubMedCentral
25.
Jiang H, Li F, He C, Wang X, Li Q, Gao H. Expression of Gli1 and Wnt2B correlates with progression and clinical outcome of pancreatic cancer. Int J Clin Exp Pathol. 2014;7:4531–8.PubMedPubMedCentral
26.
Wang H, Fan L, Xia X, Rao Y, Ma Q, Yang J, Lu Y, Wang C, Ma D, Huang X. Silencing Wnt2B by siRNA interference inhibits metastasis and enhances chemotherapy sensitivity in ovarian cancer. Int J Gynecol Cancer. 2012;22:755–61.CrossRefPubMed
27.
Iwatsuki M, Mimori K, Yokobori T, Ishi H, Beppu T, Nakamori S, Baba H, Mori M. Epithelial-mesenchymal transition in cancer development and its clinical significance. Cancer Sci. 2010;101:293–9.CrossRefPubMed
28.
Guarino M, Rubino B, Ballabio G. The role of epithelial-mesenchymal transition in cancer pathology. Pathology. 2007;39:305–18.CrossRefPubMed
29.
Yanaka Y, Muramatsu T, Uetake H, Kozaki K, Inazawa J. MiR-544a induces epithelial-mesenchymal transition through the activation of WNT signaling pathway in gastric cancer. Carcinogenesis. 2015;36:1363–71.CrossRefPubMed
30.
Baldwin LA, Hoff JT, Lefringhouse J, Zhang M, Jia C, Liu Z, Erfani S, Jin H, Xu M, She QB, van Nagell JR, Wang C, Chen L, Plattner R, Kaetzel DM, Luo J, Lu M, West D, Liu C, Ueland FR, Drapkin R, Zhou BP, Yang XH. CD151-alpha3beta1 integrin complexes suppress ovarian tumor growth by repressing slug-mediated EMT and canonical Wnt signaling. Oncotarget. 2014;5:12203–17.CrossRefPubMedPubMedCentral
31.
Vincan E, Barker N. The upstream components of the Wnt signalling pathway in the dynamic EMT and MET associated with colorectal cancer progression. Clin Exp Metastasis. 2008;25:657–63.CrossRefPubMed
32.
Liang J, Liang L, Ouyang K, Li Z, Yi X. MALAT1 induces tongue cancer cells’ EMT and inhibits apoptosis through Wnt/beta-catenin signaling pathway. J Oral Pathol Med. 2016. doi:10.​1111/​jop.​12466.
Metadata
Title
miR-324-3p suppresses migration and invasion by targeting WNT2B in nasopharyngeal carcinoma
Authors
Chao Liu
Guo Li
Nianting Yang
Zhongwu Su
Shuiting Zhang
Tengbo Deng
Shuling Ren
Shanhong Lu
Yongquan Tian
Yong Liu
Yuanzheng Qiu
Publication date
01-12-2017
Publisher
BioMed Central
Published in
Cancer Cell International / Issue 1/2017
Electronic ISSN: 1475-2867
DOI
https://doi.org/10.1186/s12935-016-0372-8

Other articles of this Issue 1/2017

Cancer Cell International 1/2017 Go to the issue

Primary Research

The role of miR-485-5p/NUDT1 axis in gastric cancer

Primary Research

ROR2 receptor promotes the migration of osteosarcoma cells in response to Wnt5a

Primary research

CBFA2T2 is associated with a cancer stem cell state in renal cell carcinoma

Primary Research

Dual EGFR and BRAF blockade overcomes resistance to vemurafenib in BRAF mutated thyroid carcinoma cells

Primary Research

ARNT is a potential direct HIF-1 target gene in human Hep3B hepatocellular carcinoma cells

Primary Research

Erythropoietin promoted the proliferation of hepatocellular carcinoma through hypoxia induced translocation of its specific receptor
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