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circRNAs in drug resistance of breast cancer 被引量:2
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作者 sema misir SERAP OZER YAMAN +3 位作者 NINA PETROVIĆ CEREN SUMER CEYLAN HEPOKUR YUKSEL ALIYAZICIOGLU 《Oncology Research》 SCIE 2022年第4期157-172,共16页
Breast cancer(BC)is the most common heterogeneous disease in women and one of the leading causes of cancer-related death.Surgery,chemotherapy,radiotherapy,hormone,and targeted therapy are the gold standards for BC tre... Breast cancer(BC)is the most common heterogeneous disease in women and one of the leading causes of cancer-related death.Surgery,chemotherapy,radiotherapy,hormone,and targeted therapy are the gold standards for BC treatment.One of the significant challenges during the treatment of BC represents resistance to chemotherapeutics,resistance that severely limits the use and effectiveness of the drugs used for BC treatment.Therefore,it is essential to develop new strategies to improve therapeutic efficacy.Circular RNAs(circRNAs)are a large group of non-coding RNAs that covalently form closed circular loops by joining their 5′,and 3′;ends.Accumulating evidence suggests that circRNAs have a vital role in cancer development,progression,and BC resistance to chemotherapy.The purpose of this review is to discuss the biological properties of circRNAs,and how circRNAs induce resistance to conventional therapeutic anti-cancer drugs used in BC treatment,by emphasizing and summarizing the potential roles of circRNAs in mechanisms of drug resistance,such as drug efflux,apoptosis dysfunction,autophagy,and DNA damage repair.CircRNAs are associated with drug resistance via ATP-binding cassette(ABC)efflux transporters,while some others by inhibition of cell apoptosis,thus leading to resistance to tamoxifen in BC cells.In contrast,others are involved in the promotion of BC cells chemoresistance by doxorubicininduced autophagy.CircRNAs may have clinical significance in regulating or overcoming BC drug resistance and may give directions towards a novel approach to personalized BC treatment.CircRNAs may significantly contribute to the identification of new therapeutic targets for the prevention of BC chemoresistance. 展开更多
关键词 Breast cancer CHEMOTHERAPY circRNAs Drug resistance Non-coding RNA
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Cytotoxic effect of Rosa canina extract on human colon cancer cells through repression of telomerase expression
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作者 Ibrahim Turan Selim Demir +7 位作者 Kagan Kilinc Serap Ozer Yaman sema misir Hanife Kara Berna Genc Ahmet Mentese Yuksel Aliyazicioglu Orhan Deger 《Journal of Pharmaceutical Analysis》 SCIE CAS CSCD 2018年第6期394-399,共6页
Rosa canina is a member of the genus Rosa that has long been used for medical objectives. Several studies have reported cytotoxic effects of different Rosa species, but there has been only limited investigation of the... Rosa canina is a member of the genus Rosa that has long been used for medical objectives. Several studies have reported cytotoxic effects of different Rosa species, but there has been only limited investigation of the cytotoxic effect of R. canina. The purpose of the current study was to examine the potential effect of R.canina extract on cell viability, the cell cycle, apoptosis, and the expression of telomerase in human colon cancer(WiDr) cells. The cytotoxic effect of the extract was determined using MTT assay. The mechanism involved in the cytotoxic effect of the extract was then evaluated in terms of apoptosis and the cell cycle using flow cytometry. Mitochondrial membrane potential(MMP) was investigated using the fluorometric method, and expression levels of telomerase were studied using RT-PCR. R. canina extract exhibited a selective cytotoxic effect on WiDr cells compared with normal colon cells. The extract induced cell cycle arrest at the S phase and apoptosis via reduced MMP in WiDr cells. R. canina extract significantly repressed telomerase expressions at treatment times of 48 and 72 h in WiDr cells. Our results suggest that R. canina may have considerable potential for development as a novel natural product-based anticancer agent. 展开更多
关键词 Apoptosis COLON cancer CYTOTOXICITY ROSA canina TELOMERASE
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