Chlorogenic acid (CA) is a phenolic compound purified from coffee, fruits and their associated beverages, which possess various biological properties, such as antioxidant and anticarcinogenic activities. The present study evaluated the effects of CA on lipopolysaccharide (LPS)‑induced inflammation in RAW264.7 cells and the associated intracellular signaling pathways using reverse transcription‑quantitative polymerase chain reaction, western blotting and enzyme‑linked immunosorbent assays. CA pretreatment inhibited LPS‑induced expression of inducible nitric oxide synthase (iNOS), nitric oxide (NO) and pro‑inflammatory mediators including interleukin (IL)‑6, tumor necrosis factor‑α (TNF‑α), macrophage inflammatory protein‑2 (MIP‑2) and IL‑1β in RAW264.7 cells. In addition, phosphorylation of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) with LPS was inhibited by CA pretreatment. CA and STAT3 inhibitor (STAT3i) pretreatment inhibited LPS‑induced nuclear translocation of phosphorylated STAT3. In addition, STAT3i inhibited the LPS‑induced expression of iNOS, NO and IL‑1β similar to the results of CA pretreatment. By contrast, STAT3i did not inhibit the LPS‑induced increase in IL‑6, TNF‑α and MIP‑2 expression. These results indicate that CA may suppress LPS‑induced NO and IL‑1β expression by inhibiting JAK2/STAT3 activation in RAW264.7 cells.

Salinomycin is a monocarboxylic polyether antibiotic, which is widely used as an anticoccidial agent. The anticancer property of salinomycin has been recognized and is based on its ability to induce apoptosis in human multidrug resistance (MDR). The present study investigated whether salinomycin reverses MDR towards chemotherapeutic agents in doxorubicin-resistant MCF-7/MDR human breast cancer cells. The results demonstrated that doxorubicin-mediated cytotoxicity was significantly enhanced by salinomycin in the MCF-7/MDR cells, and this occurred in a dose-dependent manner. This finding was consistent with subsequent observations made under a confocal microscope, in which the doxorubicin fluorescence signals of the salinomycin-treated cells were higher compared with the cells treated with doxorubicin alone. In addition, flow cytometric analysis revealed that salinomycin significantly increased the net cellular uptake and decreased the efflux of doxorubicin. The expression levels of MDR-1 and MRP-1 were not altered at either the mRNA or protein levels in the cells treated with salinomycin. These results indicated that salinomycin was mediated by its ability to increase the uptake and decrease the efflux of doxorubicin in MCF-7/MDR cells. Salinomycin reversed the resistance of doxorubicin, suggesting that chemotherapy in combination with salinomycin may benefit MDR cancer therapy.

We present an English–Korean speech translation corpus, named EnKoST‐C. End‐to‐end model training for speech translation tasks often suffers from a lack of parallel data, such as speech data in the source language and equivalent text data in the target language. Most available public speech translation corpora were developed for European languages, and there is currently no public corpus for English–Korean end‐to‐end speech translation. Thus, we created an EnKoST‐C centered on TED Talks. In this process, we enhance the sentence alignment approach using the subtitle time information and bilingual sentence embedding information. As a result, we built a 559‐h English–Korean speech translation corpus. The proposed sentence alignment approach showed excellent performance of 0.96 f‐measure score. We also show the baseline performance of an English–Korean speech translation model trained with EnKoST‐C. The EnKoST‐C is freely available on a Korean government open data hub site.

Lasalocid is an antibiotic from the group of carboxylic ionophores and is produced by Streptomyces lasaliensis. But there is limited information on the effect of lasalocid on human prostate cancer cells. In the present studies, the lasalocid was examined to better understand its effect on apoptosis and associated signal pathways in vitro in human prostate cancer cells. Using PC‐3 cells, we demonstrate that lasalocid triggers apoptosis by elevating the intracellular ROS level, which was accompanied by increased mitochondrial membrane potential, prompted the levels of Bax and caspase‐3 and reduced the level of Bcl‐2, and cleavage of PARP‐1, a caspase‐3 substrate. These results are the first to link elevated oxidative stress and mitochondrial membrane hyperpolarization to caspase‐dependent apoptosis of lasalocid‐treated prostate cancer cells.