•Lactobacillus X12 arrests HT-29 cell cycle at G1 phase.•Lactobacillus X12 inhibits the expressions of cyclin E1 mRNA and cyclin D1 mRNA.•Lactobacillus X12 induces cyclin-dependent kinases inhibitor p27.•Lactobacillus X12 suppresses the expression of mTOR.•mTOR/p27 takes the crucial roles in Lactobacillus X12-mediated cell cycle arrest.L. paracasei subp. paracasei X12 1 is obtained from traditional cheese in northwestern China and exhibited effective anticancer activities in previous screening experiments. Here, its effects on colon cancer cell line HT-29 cell cycle and the roles of mammalian target of rapamycin (mTOR) signalling were investigated. Firstly, the effects of Lactobacillus X12 at different multiplicity of infection (MOI) on HT-29 cell cycle were detected by flow cytometry. In order to determine the specific regulators involved, cyclin D1, cyclin E1, the positive regulators, and p21, p16, and p27, the negative regulatory factors, were further explored by RT-PCR technique. Finally, mTOR signalling was focused to demonstrate its relationship with cell cycle arrest. Overall, the present findings suggested that Lactobacillus X12 can block HT-29 cell cycle at G1 phase through inhibiting cyclin E1, meanwhile enhancing p27, which were mediated by mTOR/4EBP12 signalling pathway. These results will provide a theoretical basis for further development of Lactobacillus.

Bioactive compounds including polysaccharides, flavones, syringin and eleutheroside E were extracted from wild Acanthopanax senticosus to obtain purities of 88.4% ± 3.2%, 90.8% ± 2.0%, 92.5% ± 1.5% and 82.7% ± 4.7% respectively. In vitro antioxidant activities and in vivo anti-radiation activities of the compounds were investigated and compared. The results demonstrated that polysaccharides and flavones extracted from A. Senticosus were more effective than syringin and eleutheroside E in their radical scavenging activity in vitro. In vivo studies showed that polysaccharides and flavones were also effective in protecting mice from heavy ion radiation induced tissue oxidative damage. Furthermore, the activities of polysaccharides and flavones in repressing expression changes of radiation response proteins including heat shock protein, disulfide-isomerase and glutathione S-transferase, were also identified by our results. These radioprotective effects were more significant when polysaccharides and flavones were administered together.

Lactobacillus paracasei subsp. paracasei M5L (L. paracasei M5L) was isolated and co-cultured with HT-29 colon cancer cells to study its anti-colorectal cancer effects and mechanism. Using the MTT assay we found that L. paracasei M5L significantly inhibits HT-29 cell proliferation. Morphological and biochemical characteristics of apoptosis were observed and confirmed by hematoxylin and eosin (HE) staining and transmission electron microscopy (TEM). Lactobacilli could change the cell cycle distribution and induce calreticulin (CRT) translocation from the endoplasmic reticulum to the surface of the cytomembrane. We also determine that vast reactive oxygen species (ROS) were generated, while the activities of superoxide dismutase (SOD) and catalase (CAT) were noticeably diminished following L. paracasei M5L treatment. This study reveals that L. paracasei M5L induces apoptosis in HT-29 cells through ROS generation followed by CRT accompanied endoplasmic reticulum (ER) stress and S phase arrest. These results provide new insights into the possible molecular mechanism of L. paracasei M5L as a novel probiotic with the potential for further application.

•Cartilage polysaccharide (PS) induced apoptosis in MCF-7 breast cancer cells.•Caspase-8 mediated Fas signaling pathway was involved in PS-induced apoptosis.•Fas was expressed in nucleus cell membrane firstly and then on outside membrane.•NF-κB inhibitor PDTC may act as a PS antagonist to reduce the apoptosis rate.Cartilage polysaccharide (PS) was extracted from porcine cartilage to investigate its anti-tumor effect. In this study, we showed that PS induced apoptosis in MCF-7 breast cancer cells by activating the caspase-8 mediated Fas signaling pathway. The PS inhibited MCF-7 cell proliferation in a dose-dependent and time-dependent manner, and had no toxic effect on normal cells such as NIH-3T3 cells. An increase of Fas protein expression was first located on the nuclear membrane and then on the outside membrane. Cleaved caspase-8 was activated after PS treatment. NF-κB activation was not involved in the PS induced apoptosis, but the NF-κB inhibitor PDTC may act as a PS antagonist to reduce the apoptosis rate and Fas protein expression in PS-induced apoptosis in MCF-7 cells.