Microarray pathway analysis indicated that mitogen-activated protein kinase/extracellular signal-regulated kinase and insulin growth factor 1 signaling pathways were inhibited by small interfering RNA against AT‑rich interactive domain 1A in endometrial cancer

  • Authors:
    • Ye Yang
    • Wei Bao
    • Zhengyu Sang
    • Yongbing Yang
    • Meng Lu
    • Xiaowei Xi
  • View Affiliations

  • Published online on: November 24, 2017     https://doi.org/10.3892/ol.2017.7489
  • Pages: 1829-1838
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Mutations in the gene encoding AT-rich interactive domain 1A (ARID1A) are frequently observed in endometrial cancer (EC) but the molecular mechanisms linking the genetic changes remain to be fully understood. The present study aimed to elucidate the influence of ARID1A mutations on signaling pathways. Missense, synonymous and nonsense heterozygous ARID1A mutations in the EC HEC‑1‑A cell line were verified by Sanger sequencing. Mutated ARID1A small interfering RNA was transfected into HEC‑1‑A cells. Biochemical microarray analysis revealed 13 upregulated pathways, 17 downregulated pathways, 14 significantly affected disease states and functions, 662 upstream and 512 downstream genes in mutated ARID1A‑depleted HEC‑1‑A cells, among which the mitogen‑activated protein kinase/extracellular signal‑regulated kinase and insulin‑like growth factor‑1 (IGF1) signaling pathways were the 2 most downregulated pathways. Furthermore, the forkhead box protein O1 pathway was upregulated, while the IGF1 receptor, insulin receptor substrate 1 and phosphatidylinositol-4,5-bisphosphate 3‑kinase catalytic subunit b pathways were downregulated. Carcinoma tumorigenesis, tumor cell mitosis and tumor cell death were significantly upregulated disease states and functions, while cell proliferation and tumor growth were significantly downregulated. The results of the present study suggested that ARID1A may be a potential prognostic and therapeutic molecular drug target for the prevention of EC progression.
View Figures
View References

Related Articles

Journal Cover

February-2018
Volume 15 Issue 2

Print ISSN: 1792-1074
Online ISSN:1792-1082

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Yang Y, Bao W, Sang Z, Yang Y, Lu M and Xi X: Microarray pathway analysis indicated that mitogen-activated protein kinase/extracellular signal-regulated kinase and insulin growth factor 1 signaling pathways were inhibited by small interfering RNA against AT‑rich interactive domain 1A in endometrial cancer. Oncol Lett 15: 1829-1838, 2018
APA
Yang, Y., Bao, W., Sang, Z., Yang, Y., Lu, M., & Xi, X. (2018). Microarray pathway analysis indicated that mitogen-activated protein kinase/extracellular signal-regulated kinase and insulin growth factor 1 signaling pathways were inhibited by small interfering RNA against AT‑rich interactive domain 1A in endometrial cancer. Oncology Letters, 15, 1829-1838. https://doi.org/10.3892/ol.2017.7489
MLA
Yang, Y., Bao, W., Sang, Z., Yang, Y., Lu, M., Xi, X."Microarray pathway analysis indicated that mitogen-activated protein kinase/extracellular signal-regulated kinase and insulin growth factor 1 signaling pathways were inhibited by small interfering RNA against AT‑rich interactive domain 1A in endometrial cancer". Oncology Letters 15.2 (2018): 1829-1838.
Chicago
Yang, Y., Bao, W., Sang, Z., Yang, Y., Lu, M., Xi, X."Microarray pathway analysis indicated that mitogen-activated protein kinase/extracellular signal-regulated kinase and insulin growth factor 1 signaling pathways were inhibited by small interfering RNA against AT‑rich interactive domain 1A in endometrial cancer". Oncology Letters 15, no. 2 (2018): 1829-1838. https://doi.org/10.3892/ol.2017.7489