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Song,L.; Duan,P.; Gan,Y.; Li,P.; Zhao,C.; Xu,J.; Zhang,Z.; Zhou,Q.. |
MicroRNAs (miRNAs) play an important role in drug resistance and modulate the efficiency of chemotherapy. A recent study indicated that miR-340 functions as a tumor suppressor in various types of cancer. However, the role of miR-340 in chemotherapy has not been reported yet. In this study, we found that miR-340 enhanced cisplatin (CDDP)-induced cell death. Induction of miR-340-5p expression decreased the IC50 of CDDP and increased the apoptosis of CDDP-resistant MG-63 and Saos-2 cells. Moreover, miR-340-5p decreased the accumulation of MRP1 and MDR1. We further explored the mechanism underlying the promoting effects of miR-340-5p on CDDP-induced cell death. We identified a potential target of miR-340 in the 3′ untranslated region of lysophosphatidic acid... |
Tipo: Info:eu-repo/semantics/report |
Palavras-chave: Sensitivity to cisplatin; LPAATβ; MiR-340-5p; Osteosarcoma. |
Ano: 2017 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2017000500606 |
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Li,Y.; Chen,L.J.; Jiang,F.; Yang,Y.; Wang,X.X.; Zhang,Z.; Li,Z.; Li,L.. |
Hormesis is an adaptive response to a variety of oxidative stresses that renders cells resistant to harmful doses of stressing agents. Caffeic acid (CaA) is an important antioxidant that has protective effects against DNA damage caused by reactive oxygen species (ROS). However, whether CaA-induced protection is a hormetic effect remains unknown, as is the molecular mechanism that is involved. We found that a low concentration (10 μM) of CaA increased human liver L-02 cell viability, attenuated hydrogen peroxide (H2O2)-mediated decreases in cell viability, and decreased the extent of H2O2-induced DNA double-strand breaks (DSBs). In L-02 cells exposed to H2O2, CaA treatment reduced ROS levels, which might have played a protective role. CaA also activated the... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Caffeic acid; Hormesis; Antioxidants; DNA double-strand breaks; Extracellular signal-regulated kinase. |
Ano: 2015 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015000600502 |
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