Faecal calprotectin and faecal occult blood test (FOBT) were widely used in the diagnosis and assessment of intestinal inflammation in inflammatory bowel disease (IBD). Recently we identified an excellent new biomarker B cell-activating factor (BAFF) for IBD. Here in this study we compared the efficacy of faecal BAFF, calprotectin and FOBT to find the “best non-invasive marker”. Results showed that for discriminating IBD from IBS, BAFF ≥227.3 pg/ml yield 84% sensitivity, 100% specificity, 100% positive predictive value (PPV) and 64% negative predictive value (NPV) while calprotectin ≥50 µg/g yield 76% sensitivity, 93% specificity, 97% PPV and 53% NPV. FOBT yield 65% sensitivity, 93% specificity, 97% PPV and 43% NPV. Combining BAFF with calprotectin tests yield 94% sensitivity, 93% specificity, 98% PPV, 81% NPV. Faecal BAFF level showed the stronger correlation with endoscopic inflammatory score as compared to calprotectin not only in UC (correlation coefficient [r] = 0.69, p < 0.0001 vs. r = 0.58, p < 0.0001), but also in CD (r = 0.58, p < 0.0001 vs. r = 0.52, p = 0.0003). Our results indicating that faecal BAFF is a promising non-invasive biomarker in IBD differential diagnosis and monitoring of intestinal inflammation.

Triple-negative breast cancer is the most aggressive type of breast cancer, with a poor prognosis, while effective treatment options are limited. In this study, the anti-tumor effect of lupeol, a natural triterpenoid, toward breast cancer cells and the underlying mechanisms were examined. We firstly predict the primary pathways of lupeol inhibited to TNBC by a network pharmacology approach, which indicated that lupeol may inhibit TNBC via multiple signaling pathways. In addition, experimental data showed that lupeol exhibited outstanding anti-proliferative and anti-metastatic abilities in vitro and in vivo. Additional intrinsic mechanism studies revealed that lupeol might induce autophagy by inhibiting the Akt-mTOR pathway, and activating an autophagy inhibited epithelial–mesenchymal transition (EMT). This study demonstrated that lupeol could inhibit TNBC cells by inducing autophagy, suggesting lupeol as a potential treatment alternative or as a dietary supplement for TNBC, as well as offering novel insights into the anti-cancer effect of lupeol.

Excessive adiposity has long been proved to be associated with greater incidence and mortality of breast cancer in post-menopausal women. However, the effects and underlying mechanisms of human adipocytes on breast cancer cells remain largely unknown. In recent years, several reports have revealed the oncogenic role of long non-coding RNA PVT1 in breast cancer. Here, we aimed to investigate the role and underlying mechanisms of PVT1 in triple-negative breast cancer (TNBC) cells cultured with mature adipogenic medium. At first, we successfully induced adipogenic differentiation from human adipose-derived mesenchymal stem cells and collected the mature adipogenic medium to mimic excessive adiposity. Our results demonstrated that the mature adipogenic medium promoted the epithelial-mesenchymal transition, enhanced the cell viability and migration potential of TNBC cells. In addition, we proved that mature adipogenic medium affected the PVT1 expression and inhibition of the PVT1 disturbed the role of mature adipogenic medium in TNBC cells. Finally, we illustrated that repression of p21 restored the phenotype caused by PVT1 knockdown in TNBC cells treated with mature adipogenic medium. Taken together, our results demonstrated that PVT1 affected the role of mature adipogenic medium in TNBC cells via modulating p21 expression.