Open Access

Role and mechanism of PTEN in Burkitt's lymphoma

  • Authors:
    • Chuntuan Li
    • Yahong Xu
    • Pengliang Xin
    • Yan Zheng
    • Xiongpeng Zhu
  • View Affiliations

  • Published online on: January 9, 2020     https://doi.org/10.3892/or.2020.7457
  • Pages: 481-490
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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


Abstract

The aim of the present study was to explore the possible mechanisms of phosphatase and tensin homolog (PTEN) in the pathogenesis of Burkitt's lymphoma, and provide novel information that can be used in the targeted treatment of this disease. PTEN lentiviral overexpression vector and short‑hairpin PTEN silencing vectors were constructed. The effect of PTEN on the growth and proliferation of CA46 and RAJI cells was analyzed using a Cell Counting Kit‑8 assay. Apoptosis was detected by Hoechst 33342 and propidium iodide double staining. Flow cytometry was used to analyze the cell cycle. A Transwell chamber was used to detect cell migration and invasion abilities. Western blot analysis was used to detect related protein changes. The mechanism of the effect of PTEN on the biological characteristics of Burkitt's lymphoma cells was subsequently analyzed. The results revealed that PTEN inhibited the proliferation of CA46 and RAJI cells by downregulating the expression of p‑AKT, It was indicated that the upregulation of proapoptotic proteins (including Bad and Bax) induced apoptosis, regulated cyclin (including P53, P21, CDK4, CDK6, cyclin D3 and cyclin H) to inhibit cell cycle progression, and mediated epithelial‑mesenchymal transition‑like cell markers (including E‑cadherin, N‑cadherin, β‑catenin, TCF‑8, vimentin, Slug and Snail) to inhibit cell migration and invasion. In conclusion, the tumor‑suppressor gene PTEN inhibited the phosphoinositide 3‑kinase/protein kinase B (PI3K/AKT) signaling pathway and inhibited the proliferation and migration of Burkitt's lymphoma cells, induced apoptosis and cell cycle arrest, thus playing a crucial role in the pathogenesis of Burkitt's lymphoma.
View Figures
View References

Related Articles

Journal Cover

February-2020
Volume 43 Issue 2

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
Li C, Xu Y, Xin P, Zheng Y and Zhu X: Role and mechanism of PTEN in Burkitt's lymphoma. Oncol Rep 43: 481-490, 2020
APA
Li, C., Xu, Y., Xin, P., Zheng, Y., & Zhu, X. (2020). Role and mechanism of PTEN in Burkitt's lymphoma. Oncology Reports, 43, 481-490. https://doi.org/10.3892/or.2020.7457
MLA
Li, C., Xu, Y., Xin, P., Zheng, Y., Zhu, X."Role and mechanism of PTEN in Burkitt's lymphoma". Oncology Reports 43.2 (2020): 481-490.
Chicago
Li, C., Xu, Y., Xin, P., Zheng, Y., Zhu, X."Role and mechanism of PTEN in Burkitt's lymphoma". Oncology Reports 43, no. 2 (2020): 481-490. https://doi.org/10.3892/or.2020.7457