Open Access

MicroRNA‑23a acts as an oncogene in pancreatic carcinoma by targeting TFPI‑2

  • Authors:
    • Wei Wang
    • Jin‑Zhuo Ning
    • Zhi‑Gang Tang
    • Ying He
    • Li-Chao Yao
    • Lin Ye
    • Lun Wu
  • View Affiliations

  • Published online on: September 4, 2020     https://doi.org/10.3892/etm.2020.9181
  • Article Number: 53
  • Copyright: © Wang 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

Pancreatic carcinoma (PC) is a rapidly progressive, fatal malignant tumor with the poorest prognosis among all major carcinoma types. MicroRNAs (miRNAs/miRs) have been indicated to be key post‑transcriptional regulatory factors, which are involved in cancer development. The present study was designed to investigate the effect of miR‑23a on PC cell proliferation, metastasis and apoptosis. The expression of miR‑23a was detected in a normal pancreatic ductal epithelial cell line and three PC cell lines, and miR‑23a inhibitor or mimics were transfected into the Panc‑1 and MiaPaCa2 PC cells. The association between miR‑23a and tissue factor pathway inhibitor (TFPI)‑2 was examined using a luciferase reporter assay. MTT and flow cytometry assays were used to assess cell viability and apoptosis, respectively. Furthermore, wound‑healing, Transwell and Matrigel assays were used to evaluate cell migration and invasion abilities, and the protein expression level of TFPI‑2 was determined using western blot analysis. The results of the present study revealed that miR‑23a was upregulated in PC cells. Furthermore, TFPI‑2 was identified as a downstream target of miR‑23a, and TFPI‑2 expression was found to be increased following miR‑23a knockdown. In addition, functional assays revealed that downregulation of miR‑23a decreased PC cell proliferation, migration and invasiveness and promoted cell apoptosis, while miR‑23a overexpression exerted the opposite effects. Furthermore, TFPI‑2 knockdown rescued the biological effects on PC cells, which were induced by miR‑23a knockdown. The results of the present study indicated that miR‑23a negatively modulated TFPI‑2 expression in vitro and enhanced the malignant phenotypes of PC cells. Therefore, miR‑23a may be a potential marker and/or target for the diagnosis and treatment of PC.
View Figures
View References

Related Articles

Journal Cover

November-2020
Volume 20 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Wang W, Ning JZ, Tang ZG, He Y, Yao L, Ye L and Wu L: MicroRNA‑23a acts as an oncogene in pancreatic carcinoma by targeting TFPI‑2. Exp Ther Med 20: 53, 2020.
APA
Wang, W., Ning, J., Tang, Z., He, Y., Yao, L., Ye, L., & Wu, L. (2020). MicroRNA‑23a acts as an oncogene in pancreatic carcinoma by targeting TFPI‑2. Experimental and Therapeutic Medicine, 20, 53. https://doi.org/10.3892/etm.2020.9181
MLA
Wang, W., Ning, J., Tang, Z., He, Y., Yao, L., Ye, L., Wu, L."MicroRNA‑23a acts as an oncogene in pancreatic carcinoma by targeting TFPI‑2". Experimental and Therapeutic Medicine 20.5 (2020): 53.
Chicago
Wang, W., Ning, J., Tang, Z., He, Y., Yao, L., Ye, L., Wu, L."MicroRNA‑23a acts as an oncogene in pancreatic carcinoma by targeting TFPI‑2". Experimental and Therapeutic Medicine 20, no. 5 (2020): 53. https://doi.org/10.3892/etm.2020.9181