Psammplysin F increased chemotherapy sensitivity to Doxorubicin by reducing the number of Stress Granules

Backgrounds: Doxorubicin (DXR) is an antibiotic derived from the bacterium Streptomycespeucetius. Since the ۱۹۶۰s, it has been widely used as a chemotherapeutic agent in theanthracycline class. DXR is commonly used in chemotherapeutic regimens with other agentsbecause of its effectiveness in destroying malignant cells. DXR's anti-tumor properties aremediated by DNA intercalation and topoisomerase inhibition. Cancer cells alone can withstandmuch stress due to maximal growth conditions; DXR also imposes increased ER stress and proapoptoticprocesses on the treated cancer cell, promoting the development of Stress Granules(SGs). An established cell mechanism for reducing the damage of stress and increasing cellsurvival involves the formation of SGs. Ribonucleoproteins is formed due to the cell's stresscaused by a break in translation. DXR, in particular, increases the number of SGs by directlyaffecting eIF۲α phosphorylation and results in its chemotherapy resistance.Materials and Methods: The number of SGs in doxorubicin-resistant cancer cells wasdetermined using the protein markers G۳BP۱ and TIA-۱. Psammplysin F, which reduces eIF۲αphosphorylation, was used to reduce the number of SGs. The sensitivity to the chemotherapydrug DXR was measured before and after the use of Psammplysin F.Results: Psammplysin F reduced the number of SGs in DXR-resistant cells while increasingsensitivity to this chemotherapeutic drug when used in combination.Conclusion: Psammplysin F reduced the number of SGs in DXR-resistant cells while increasingsensitivity to this chemotherapeutic drug when used in combination. Psammplysin F can be usedas the primary compound to improve DXR efficiency in cancer-resistant cells.

کلیدواژه ها:

Doxorubicin ، Stress granule ، Psammplysin F ، Cancer ، G۳BP۱