We aimed to investigate the possible anticancer effects of radiation in combination with 17‐allylamino‐17‐demethoxy geldanamycin (17‐AAG) and silver graphene quantum dot (SQD) in breast cancer (BC) cells. MCF‐7 BC cells treated with, or without, different concentrations of 17‐AAG and synthesized SQD and cellular viability detected. The growth inhibitory effects of low concentrations of 17‐AAG with minimally toxic concentration of SQD in combination with 2 Gy of X‐ray radiation were examined. The apoptosis induction assessed by acridine orange/ethedium bromide staining. Likewise, the levels of lactate, hydrogen peroxide (H2O2), nitric oxide (NO) were evaluated. The relative gene expression levels of Bax and Bcl‐2 were detected by real‐time polymerase chain reaction and the Bax/Bcl‐2 expression ratio was determined. Moreover, the protein expression of epidermal growth factor receptor (EGFR) was assessed by western blot analysis. Treatment with low concentrations of 17‐AAG and SQD at a minimally toxic concentration promoted inhibition of BC cell growth and induced apoptosis. In addition, significant reduction in cell viability was seen in triple combination versus all double and single treatments. Indeed 17‐AAG and SQD in combined with radiation significantly increased the H2O2 and NO versus single and double treated cases. In addition, triple combination treatment showed decreased lactate level in compared tomonotherapies. EGFR protein expression levels were found to decreased in all double and triple combined cases versus single treatments. Additionally, in double and triple treatments, Bax/Bcl2 ratio were higher in compared to single treatments. Treatment with low concentrations of 17‐AAG and SQD at a minimally toxic concentration tends to induce anticancer effects and increase the radiation effects when applied with 2 Gy of radiation versus radiation monotherapy.

Purpose: Apatinib has been utilized in colon cancer therapies but its efficiency and molecular mechanism are not fully understood. Chemotherapy in combination with non-toxic compounds can be a strategy to reduce the recurrence of cancer. Consequently, this study was carried out to evaluate the effects of Apatinib and Piperine on colorectal cancer (CRC) cell line and their potential anti-cancerous mechanisms in vitro. Methods: The effects of Apatinib and Piperine on HCT-116 CRC cells were detected by assessing cell viability using MTT assay. The potential cytotoxic mechanisms of Apatinib and Piperine were investigated by evaluating the apoptosis-related gene (MDM-2) expression ratio using real-time PCR assay. Moreover, the glutathione peroxidase activity (GPX) and nitric oxide (NO) levels were assessed by colorimetric assays. Results: The proliferation rate of CRC cells decreased by increasing the concentrations of Piperine and Apatinib. When HCT-116 cells were treated with different concentrations of Apatinib in combination with Piperine, the synergistic effects were observed (Combination Index<1). In HCT-116 cells treated with Apatinib or Piperine at the concentrations of 0.5×IC50 and 0.2×IC50, the MDM-2 gene expression was downregulated and NO levels increased compared to the untreated control cells and related single treatments. Furthermore, the cytotoxic effects of Apatinib increased when was combined with Piperine. In addition, GPX activity significantly decreased in combination treatment at 0.5×IC50 concentration of both agents. Conclusion: Apatinib in combination with Piperin could significantly inhibit the viability of CRC cells. These cytotoxic effects were induced by regulation of apoptosis-related gene and inhibition of antioxidant marker.