PubMed_ArguminSci  

PubMed:28260110 JSONTXT 29 Projects

Annnotations TAB TSV DIC JSON TextAE

Id Subject Object Predicate Lexical cue
T1 94-237 DRI_Background denotes Fatty acid synthase (FASN) is a key anabolic enzyme for de novo fatty acid synthesis, which is important in the development of colon carcinoma.
T2 238-334 DRI_Challenge denotes The high expression of FASN is considered a promising molecular target for colon cancer therapy.
T3 335-532 DRI_Challenge denotes Emodin, a naturally occurring anthraquinone, exhibits an anticancer effect in various types of human cancer, including colon cancer; however, the molecular mechanisms remain to be fully elucidated.
T4 533-596 DRI_Approach denotes Cell viability was evaluated using a Cell Counting Kit‑8 assay.
T5 597-705 DRI_Background denotes The apoptosis rate of cells was quantified via flow cytometry following Annexin V/propidium iodide staining.
T6 706-929 DRI_Background denotes FASN activity was measured by monitoring oxidation of nicotinamide adenine dinucleotide phosphate at a wavelength of 340 nm, and intracellular free fatty acid levels were detected using a Free Fatty Acid Quantification kit.
T7 930-1059 DRI_Background denotes Western blot analysis and reverse transcription‑polymerase chain reaction were used to detect target gene and protein expression.
T8 1060-1228 DRI_Background denotes The present study was performed to investigate whether the gene expression of FASN and its enzymatic activity are regulated by emodin in a human colon cancer cell line.
T9 1229-1392 DRI_Background denotes Emodin markedly inhibited the proliferation of HCT116 cells and a higher protein level of FASN was expressed, compared with that in SW480, SNU-C2A or SNU‑C5 cells.
T10 1393-1555 DRI_Background denotes Emodin significantly downregulated the protein expression of FASN in HCT116 cells, which was caused by protein degradation due to elevated protein ubiquitination.
T11 1556-1673 DRI_Background denotes Emodin also inhibited intracellular FASN enzymatic activity and reduced the levels of intracellular free fatty acids.
T12 1674-1759 DRI_Background denotes Emodin enhanced antiproliferation and apoptosis in a dose‑ and time‑dependent manner.
T13 1760-1880 DRI_Background denotes The combined treatment of emodin and cerulenin, a commercial FASN inhibitor, had an additive effect on these activities.
T14 1881-1979 DRI_Approach denotes Palmitate, the final product of the FASN reaction, rescued emodin‑induced viability and apoptosis.
T15 1980-2115 DRI_Background denotes In addition, emodin altered FASN‑involved signaling pathways, including phosphatidylinositol 3-kinase/Akt and mitogen‑activated protein
T16 2155-2167 DRI_Background denotes kinases 1/2.
T17 2168-2328 DRI_Background denotes These results suggested that emodin-regulated cell growth and apoptosis were mediated by inhibiting FASN and provide a molecular basis for colon cancer therapy.