Objective: The function of Ras-related C3 botulinum toxin substrate1 (Rac1) in the progression of cervical cancer is unclear. This study used RNA interference technology to explore the involvement of Rac1 in the regulation of cervical cancer cells.
Methods: A short hairpin (sh) RNA plasmid targeting Rac1 was constructed and transfected into HeLa cells. Rac1 mRNA and protein levels were investigated by reverse transcription-polymerase chain reaction and Western blot, respectively. Cell proliferation and cisplatin chemosensitivity were determined using the methyl thiazolyl tetrazolium assay. The Matrigel™ assay and flow cytometry were used to assess cell invasion and apoptosis, respectively. The concentration of matrix metalloproteinase (MMP)-2 in cell supernatants was detected by enzyme-linked immunosorbent assay.
Results: Rac1 expression was significantly downregulated at the mRNA and protein levels in HeLa cells transfected with Rac1 shRNA, and the cell proliferation and invasion capability of cells was decreased. Rac1 downregulation was associated with a decrease in MMP-2 secretion, and increased cell chemosensitivity to cisplatin and cisplatin-induced apoptosis.
Conclusions: Rac1 may play an important role in cervical cancer progression and could be a potential target for anticancer therapy.
Keywords: RNA interference (RNAi); Ras-related C3 botulinum toxin substrate1 (Rac1); cell proliferation; cervical cancer; chemosensitivity; invasion.