Small interfering RNA-induced inhibition of epithelial cell transforming sequence 2 suppresses the proliferation, migration and invasion of osteosarcoma cells Retraction in /10.3892/etm.2021.10408

Xie,Jie; Lei,Pengfei; Hu,Yihe

doi:10.3892/etm.2015.2306

Small interfering RNA-induced inhibition of epithelial cell transforming sequence 2 suppresses the proliferation, migration and invasion of osteosarcoma cells

Retraction in: /10.3892/etm.2021.10408

Authors:
- Jie Xie
- Pengfei Lei
- Yihe Hu
View Affiliations

Affiliations: Department of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China
Published online on: February 20, 2015 https://doi.org/10.3892/etm.2015.2306
Pages: 1881-1886

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

Osteosarcoma (OS) is the most common malignant tumor in bones. Although the five‑year survival rate has improved to ~60% for patients without metastasis, the prognosis remains poor for patients with metastatic OS. Epithelial cell transforming sequence 2 (ECT2) has been shown to act as an oncogene in human malignancies. More recently, ETC2 was shown to be involved in the development and progression of OS; however, the detailed role of ECT2 in the regulation of cellular biological processes in OS cells remains largely unknown. Therefore, it was investigated in the present study. It was found that the expression of ECT2 was notably increased in OS tissues when compared with that in matched normal adjacent tissues. Furthermore, it was established that the downregulation of ECT2 induced by transfection with ECT2‑specific small interfering RNA effectively inhibited OS cell proliferation and induced cell apoptosis. Further investigation revealed that the inhibition of ECT2 expression suppressed OS cell migration and invasion, indicating that the overexpression of ECT2 promotes OS cell migration and invasion, while. In addition, western blotting results indicated that matrix metalloproteinases 2 and 9 may be involved in the ECT2‑mediated OS cell invasion. In conclusion, the current study suggested that ECT2 acted as an oncogene in OS, and it may become a promising therapeutic target for the prevention and treatment of OS.

View Figures

View References

1	De Boer Posthuma J, Witlox MA, Kaspers GJ and van Royen BJ: Molecular alterations as target for therapy in metastatic osteosarcoma: a review of literature. Clin Exp Metastasis. 28:493–503. 2011. View Article : Google Scholar : PubMed/NCBI
2	Liang W, Gao B, Fu P, Xu S, Qian Y and Fu Q: The miRNAs in the pathogenesis of osteosarcoma. Front Biosci (Landmark Ed). 18:788–794. 2013. View Article : Google Scholar : PubMed/NCBI
3	Tatsumoto T, Xie X, Blumenthal R, Okamoto I and Miki T: Human ECT2 is an exchange factor for rho GTpases, phosphorylated in G2/M phases and involved in cytokinesis. J Cell Biol. 147:921–928. 1999. View Article : Google Scholar : PubMed/NCBI
4	Salhia B, Tran NL, Chan A, et al: The guanine nucleotide exchange factors trio, Ect2 and Vav3 mediate the invasive behavior of glioblastoma. Am J Pathol. 173:1828–1838. 2008. View Article : Google Scholar : PubMed/NCBI
5	Miki T, Smith CL, Long JE, Eva A and Fleming TP: Oncogene ect2 is related to regulators of small GTP-binding proteins. Nature. 362:462–465. 1993. View Article : Google Scholar : PubMed/NCBI
6	Fields AP and Justilien V: The guanine nucleotide exchange factor (GEF) Ect2 is an oncogene in human cancer. Adv Enzyme Regul. 50:190–200. 2010. View Article : Google Scholar : PubMed/NCBI
7	Murata Y, Minami Y, Iwakawa R, et al: ECT2 amplification and overexpression as a new prognostic biomarker for early-stage lung adenocarcinoma. Cancer Sci. 105:490–497. 2014. View Article : Google Scholar : PubMed/NCBI
8	Xu J, Yao Q, Hou Y, et al: Mir-223/ect2/p21 signaling regulates osteosarcoma cell cycle progression and proliferation. Biomed Pharmacother. 67:381–386. 2013. View Article : Google Scholar : PubMed/NCBI
9	Zhang H, Yin Z, Ning K, Wang L, Guo R and Ji Z: Prognostic value of microRNA-223/epithelial cell transforming sequence 2 signaling in patients with osteosarcoma. Hum Pathol. 45:1430–1436. 2014. View Article : Google Scholar : PubMed/NCBI
10	Yang YL, Chu JY, Luo ML, et al: Amplification of PRKCI, located in 3q26, is associated with lymph node metastasis in esophageal squamous cell carcinoma. Genes Chromosomes Cancer. 47:127–136. 2008. View Article : Google Scholar : PubMed/NCBI
11	Hussenet T, Dali S, Exinger J, et al: SOX2 is an oncogene activated by recurrent 3q26.3 amplifications in human lung squamous cell carcinomas. PLoS One. 5:e89602010. View Article : Google Scholar : PubMed/NCBI
12	Wang Y, Hill KS and Fields AP: PKCiota maintains a tumor-initiating cell phenotype that is required for ovarian tumorigenesis. Mol Cancer Res. 11:1624–1635. 2013. View Article : Google Scholar : PubMed/NCBI
13	Nalini V, Segu R, Deepa PR, Khetan V, Vasudevan M and Krishnakumar S: Molecular insights on post-chemotherapy retinoblastoma by microarray gene expression analysis. Bioinform Biol Insights. 7:289–306. 2013. View Article : Google Scholar : PubMed/NCBI
14	Samuel N, Sayad A, Wilson G, et al: Integrated genomic, transcriptomic and RNA-interference analysis of genes in somatic copy number gains in pancreatic ductal adenocarcinoma. Pancreas. 42:1016–1026. 2013. View Article : Google Scholar : PubMed/NCBI
15	Vazquez-Mena O, Medina-Martinez I, Juarez-Torres E, et al: Amplified genes may be overexpressed, unchanged, or downregulated in cervical cancer cell lines. PLoS One. 7:e326672012. View Article : Google Scholar : PubMed/NCBI
16	Jung Y, Lee S, Choi HS, et al: Clinical validation of colorectal cancer biomarkers identified from bioinformatics analysis of public expression data. Clin Cancer Res. 17:700–709. 2011. View Article : Google Scholar : PubMed/NCBI
17	Iyoda M, Kasamatsu A, Ishigami T, et al: Epithelial cell transforming sequence 2 in human oral cancer. PLoS One. 5:e140822010. View Article : Google Scholar : PubMed/NCBI
18	Etienne-Manneville S and Hall A: Rho GTPases in cell biology. Nature. 420:629–635. 2002. View Article : Google Scholar : PubMed/NCBI
19	Boettner B and Van Aelst L: The role of rho GT pases in disease development. Gene. 286:155–174. 2002. View Article : Google Scholar : PubMed/NCBI
20	Fortin SP, Ennis MJ, Schumacher CA, et al: Cdc42 and the guanine nucleotide exchange factors ect2 and trio mediate fn14-induced migration and invasion of glioblastoma cells. Mol Cancer Res. 10:958–968. 2012. View Article : Google Scholar : PubMed/NCBI
21	Sano M, Genkai N, Yajima N, et al: Expression level of ECT2 proto-oncogene correlates with prognosis in glioma patients. Oncol Rep. 16:1093–1098. 2006.PubMed/NCBI
22	Justilien V, Jameison L, Der CJ, Rossman KL and Fields AP: Oncogenic activity of Ect2 is regulated through protein kinase C iota-mediated phosphorylation. J Biol Chem. 286:8149–8157. 2011. View Article : Google Scholar : PubMed/NCBI