Increased expression of ZNF 703 in breast cancer tissue: An opportunity for RNAi-NSAID combinatorial therapy

Area of Science:

• Oncology
• Molecular Biology
• Pharmacology

Background:

• Zinc finger protein 703 (ZNF703) is an oncogene linked to apoptosis and chemotherapy resistance in breast cancer.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) possess known antitumor activities.
• Cyclooxygenase-2 (COX-2) is a key target in NSAID research.

Purpose of the Study:

• To compare ZNF703 expression in breast cancer versus healthy tissue and cell lines.
• To investigate the combined therapeutic effect of anti-ZNF703 RNA interference (RNAi) and ibuprofen on breast cancer cells.
• To evaluate the impact of these treatments on cell survival and apoptosis.

Main Methods:

• Real-time PCR was used to quantify ZNF703 expression levels.
• MCF-7 breast cancer cells were treated with anti-ZNF703 RNAi and ibuprofen, individually and in combination.
• Cell viability, apoptosis, mitochondrial membrane potential, and specific protein markers (BAX, LC3A) were assessed.

Main Results:

• ZNF703 expression was significantly elevated (93.3% in tissue, fourfold in cell line) in breast cancer.
• Ibuprofen inhibited MCF-7 cell viability in a dose-dependent manner.
• Combined treatment with ibuprofen and anti-ZNF703 RNAi demonstrated enhanced apoptosis induction and reduced ZNF703 expression compared to monotherapy.

Conclusions:

• The combination of ibuprofen (a COX-2 inhibitor) and anti-ZNF703 RNAi exhibits significant therapeutic potential for breast cancer.
• This combined approach effectively inhibits breast cancer cell proliferation and promotes apoptosis.
• Targeting ZNF703 alongside COX-2 inhibition offers a promising strategy for breast cancer treatment.