Flap endonuclease 1 silencing is associated with increasing the cisplatin sensitivity of SGC‑7901 gastric cancer cells.

Flap endonuclease 1 silencing is associated with increasing the cisplatin sensitivity of SGC‑7901 gastric cancer cells. Mol Med Rep. 2016 Jan;13(1):386-92 Authors: Xie C, Wang K, Chen D Abstract Flap endonuclease 1 (FEN1), which is key in DNA replication and repair, has been demonstrated to be intimately involved in the development and progression of cancer. Our previous study determined that the downregulation of FEN1 can suppress the proliferation of, and induce apoptosis in, gastric cancer SGC‑7901 cells. In addition, several FEN1 inhibitors have been identified to increase sensitisation to DNA injury agents. These results may provide a promising treatment method to enhance the traditional chemotherapeutics used for the treatment of gastric cancer. Thus, the aim of the present study was to determine the role of FEN1 in the chemosensitivity of SGC‑7901 cells. The protein expression levels of FEN1 in cisplatin (CDDP)‑treated SGC‑7901 cells were detected using western blot analysis. FEN1 was silenced via specific FEN1‑targeted small interfering RNAs (siRNA). The survival and apoptotic rates of the SGC‑7901 cells were assessed using an MTT assay and flow cytometry, respectively. Relevant apoptotic factors were detected using western blotting. The results showed that the expression of FEN1 was significantly induced by CDDP in a dose‑ and time‑dependent manner. The targeting of FEN1 in SGC‑7901 cells, in combination...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research