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Phosphatidylcholine (PC) has been demonstrated as anti-inflammatory and antioxidant/pro-oxidant molecules. In this study, we investigated the protective effects of PC on inflammatory bowel disease (IBD) caused by lipopolysaccharide (LPS)-induced injury in intestinal epithelia cells. The IEC-6 cells (intestinal epithelia cells) were stimulated with LPS (1 μg/mL) for 24 h with or without PC pretreatment, in the next steps: (1) the level of the inflammatory cytokine tumor necrosis factor (TNF)-α was measured with ELISA; (2) the nuclear translocation and phosphorylation of NF-κB was investigated with Western blot, EMSA, immunofluorence assay; (3) the protein phosporylation levels in MAPK signaling pathway were detected with Western blot method. The results showed: (1) compared with the normal group, 10 and 20 μg/mL of PC significantly inhibited the production and activation of TNF-α, (P  <  0.01); (2) pretreatment with PC inhibited LPS-induced nuclear translocation and phosphorylation of p65 in IEC-6 cells; (3) pretreatment with PC inhibited the protein phosphorylation levels in MAPK signaling pathway. Our findings indicated that PC had the effect to protect IEC-6 cells from LPS-induced injury and this effect was exerted possibly through inhibiting the TNF-ɑ secretion, down-regulating nuclear translocation and phosphorylation of p65 and inhibiting MAPK signaling pathways. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is a prevalent malignant tumor with high morbidity and mortality across the world. Recent findings have suggested that long noncoding (lnc)RNA HOXA-AS3 plays an important role in tumorigenesis and metastasis in a variety of cancers. However, the role of lncRNA HOXA-AS3 in the initiation and progression of HCC remains largely unclear. In the present study, HOXA-AS3 was highly expressed in HCC tumor tissues and cell lines. High HOXA-AS3 expression was correlated with low survival of HCC patients. Loss-of-function experiments showed that knockdown of HOXA-AS3 inhibited cell proliferation, migration, invasion, the epithelial-mesenchymal transition (EMT) process, and the mitogen-activated protein kinase/extracellular regulated protein kinase (MEK/ERK) signaling pathway in HCC. Molecular mechanism exploration uncovered that HOXA-AS3 could directly interact with and negatively regulate miR-29c . BMP1 is a downstream target gene of miR-29c , and HOXA-AS3 could regulate BMP1 expression by targeting miR-29c . miR-29c negatively regulated and BMP1 promoted the progression of HCC. Rescue experiments revealed that miR-29c inhibitor could partially counteract the impact induced by HOXA-AS3 knockdown in HCC. Taken together, our study is the first to show the interaction of HOXA-AS3 with miR-29c in facilitating cell proliferation, metastasis, EMT process, and MEK/ERK signaling pathway in HCC.