Open Access

ARPC2 promotes breast cancer proliferation and metastasis

  • Authors:
    • Zhongle Cheng
    • Wei Wei
    • Zhengshen Wu
    • Jing Wang
    • Xiaojuan Ding
    • Youjing Sheng
    • Yinli Han
    • Qiang Wu
  • View Affiliations

  • Published online on: April 12, 2019     https://doi.org/10.3892/or.2019.7113
  • Pages: 3189-3200
  • Copyright: © Cheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 4.0].

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


Abstract

Actin-related protein 2/3 complex (ARPC2) is an actin‑binding component involved in the regulation of actin polymerization. It mediates the formation of branched actin networks and contacts the mother actin filament. Migration and invasion are key processes which enable tumor cells to infiltrate blood vessels or lymphatic vessels, and the actin pathway plays a very important role. Given that ARPC2 is critical to this progression, the present study focused on ARPC2 activity in breast cancer (BrCa) cell invasion and migration. Limited data are available on the expression and role of ARPC2 proteins in breast carcinomas. We screened the Oncomine database for messenger RNAs (mRNAs) that are upregulated in BrCa and found that ARPC2 was one of the most consistently involved mRNAs in BrCa. The analysis of immunohistochemical data revealed that ARPC2 expression was higher in breast cancerous tissues than in adjacent non‑cancerous tissues. In addition, ARPC2 was highly associated with the tumor stage, nodal metastasis, and overall survival of patients with BrCa. We performed siRNA‑ARPC2 transfection to investigate the effect of ARPC2 on the proliferation, migration, invasion and arrest of BrCa cells. It was revealed that ectopic ARPC2 expression significantly upregulated N‑cadherin, vimentin, ZEB1, MMP‑9 and MMP‑3 expression and also activated the TGF‑β pathway to contribute to epithelial‑mesenchymal transition (EMT). These results collectively indicated that ARPC2 promoted the tumorigenesis of breast carcinoma and the initiation of EMT. Therefore, ARPC2 was revealed to be a potential therapeutic target in patients with BrCa.
View Figures
View References

Related Articles

Journal Cover

June-2019
Volume 41 Issue 6

Print ISSN: 1021-335X
Online ISSN:1791-2431

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Cheng Z, Wei W, Wu Z, Wang J, Ding X, Sheng Y, Han Y and Wu Q: ARPC2 promotes breast cancer proliferation and metastasis. Oncol Rep 41: 3189-3200, 2019
APA
Cheng, Z., Wei, W., Wu, Z., Wang, J., Ding, X., Sheng, Y. ... Wu, Q. (2019). ARPC2 promotes breast cancer proliferation and metastasis. Oncology Reports, 41, 3189-3200. https://doi.org/10.3892/or.2019.7113
MLA
Cheng, Z., Wei, W., Wu, Z., Wang, J., Ding, X., Sheng, Y., Han, Y., Wu, Q."ARPC2 promotes breast cancer proliferation and metastasis". Oncology Reports 41.6 (2019): 3189-3200.
Chicago
Cheng, Z., Wei, W., Wu, Z., Wang, J., Ding, X., Sheng, Y., Han, Y., Wu, Q."ARPC2 promotes breast cancer proliferation and metastasis". Oncology Reports 41, no. 6 (2019): 3189-3200. https://doi.org/10.3892/or.2019.7113