SLC1A3 knockdown in inhibiting the proliferation, apoptosis resistance, and migration of ovarian cancer cells.

Abstract

Background: Ovarian cancer accounts for 3% of all malignancies in women and kills about 140,000 women worldwide each year, representing the fifth leading cause of cancer-related death in women. At diagnosis, 70% of patients with ovarian cancer are already at stage III or IV disease, with a 5-year survival rate of less than 45%. Studies have found that solute carrier family 1 member 3 (SLC1A3) is highly expressed in various cancers and is associated with the poor prognosis of these cancers. However, the role of SLC1A3 in ovarian cancer remains unknown. The purpose of this study was to investigate the role of the SLC1A3 gene in the proliferation, apoptosis, migration, and outcomes of ovarian cancer.

Methods: The expression level of SLC1A3 was measured via quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Knockdown experiments were performed with small interfering RNA targeting SLC1A3 in ovarian cancer cells. After the knockdown of SLC1A3, proliferation was evaluated with Cell Counting Kit 8 (CCK8) assay, apoptosis was measured by flow cytometry, and migration was evaluated via wound-healing assay. Kaplan-Meier method was used to analyze the effect of SLC1A3 expression on the prognosis of patients with ovarian cancer.

Results: High expression of SLC1A3 was associated with poor prognosis in ovarian cancer patients, and the expression of SLC1A3 in ovarian cancer cells was higher than that in ovarian epithelial cells. In vitro experiments demonstrated that knockdown of SLC1A3 restrained the proliferation activity of ovarian cancer cells, enhanced cell apoptosis, and inhibited cell migration.

Conclusions: High expression of SLC1A3 is linked to poor prognosis in ovarian cancer patients. SLC1A3 activity impedes apoptosis while enhancing the proliferation and migration of ovarian cancer cells, suggesting its potential as a therapeutic target for drug development.