HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer

Oncol Rep. 2023 Mar;49(3):64. doi: 10.3892/or.2023.8501. Epub 2023 Feb 17.

Abstract

HOXA cluster antisense RNA 3 (HOXA‑AS3) is considered to be involved in several malignancies, however, its biological function in the progression of epithelial ovarian cancer (EOC) remains unclear. The present study compared the expression of HOXA‑AS3 in ovarian cancer and normal ovarian tissues and analyzed the association between the expression of HOXA‑AS3 and the survival outcomes of patients with ovarian cancer. RNA interference was used to suppress HOXA‑AS3 expression in ovarian cancer cell lines in order to demonstrate the function of HOXA‑AS3 in ovarian cancer progression. The associations between HOXA‑AS3 and epithelial‑mesenchymal transition (EMT) markers were explored to verify the mechanism of action of HOXA‑AS3 in ovarian cancer. The results of the present study revealed that ovarian cancer tissues exhibited higher HOXA‑AS3 expression than normal ovarian tissues. Clinical data indicated that HOXA‑AS3 was a significant predictor of progression‑free survival and overall survival. Patients with high HOXA‑AS3 expression had a poorer prognosis than patients with low HOXA‑AS3 expression. In vitro experiments using HOXA‑AS3‑knockdown ovarian cancer cell lines demonstrated that HOXA‑AS3 knockdown inhibited cell proliferation and migration. HOXA‑AS3 was a potent inducer and modulator of the expression of EMT pathway‑related markers and interacted with both the mRNA and protein forms of HOXA3. Collectively, the findings of the present study demonstrated that HOXA‑AS3 expression is associated with ovarian cancer progression and thus, may be employed as a prognostic marker and therapeutic target in EOC.

Keywords: HOXA‑AS3; long noncoding RNA; ovarian cancer; prognosis; progression.

MeSH terms

  • Carcinoma, Ovarian Epithelial / pathology
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Epithelial-Mesenchymal Transition / genetics
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Ovarian Neoplasms* / pathology
  • Prognosis
  • RNA, Long Noncoding* / genetics

Substances

  • RNA, Long Noncoding

Grants and funding

The present study was supported by a research grant from Yongin Severance Hospital, Yonsei University College of Medicine.