Wang Z, Chen K, Zhang K, He K, Zhang D, Guo X, Huang T, Hu J, Zhou X, Nie S Agrocybe cylindracea fucoglucogalactan induced lysosome-mediated apoptosis of colorectal cancer cell through H3K27ac-regulated cathepsin D Carbohydrate Polymers319 (2023)
121208
/Variants 0/-+
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-6)-a-Galp-(1-6)-a-Galp-(1-6)-b-Glcp-(1-6)-b-Glcp-(1-6)-b-Glcp-(1-
/Variants 0/ is:
b-Glcp-(1-2)-
OR (exclusively)
a-Fucp-(1-2)-
NCBI PubMed ID:37567726 Publication DOI:10.1016/j.carbpol.2023.121208 Journal NLM ID:8307156 Publisher: Elsevier Correspondence: X. Zhou <zhouxingtaoncu.edu.cn>; S. Nie <spniencu.edu.cn> Institutions: State Key Laboratory of Food Science and Technology, China-Canada Joint Laboratory of Food Science and Technology (Nanchang), Nanchang University, Nanchang 330047, China
Inducing lysosomal dysfunction is emerging as a promising means for cancer therapy. Agrocybe cylindracea fucoglucogalactan (ACP) is a bioactive ingredient with anti-tumor activity, while its mechanism remains obscure. Herein, we found that ACP visibly inhibited the proliferation of colorectal cancer cells, and the IC50 value on HCT-116 cells (HT29 cells) was 490 μg/mL (786.4 μg/mL) at 24 h. RNA-seq showed that ACP regulated mitochondria, lysosome and apoptosis-related pathways. Further experiments proved that ACP indeed promoted apoptosis and lysosomal dysfunction of HCT-116 cells. Moreover, ChIP-seq revealed that ACP increased histone-H3-lysine-27 acetylation (H3K27ac) on CTSD (cathepsin D) promoter in HCT-116 cells, thus facilitating the binding of transcription factor EB (TFEB), and resulted in ascension of CTSD expression. Additionally, ACP triggered mitochondrial-mediated apoptosis by decreasing mitochondrial membrane potential and increasing pro-apoptotic protein levels. Notably, Pepstatin A (CTSD inhibitor) availably alleviated ACP-induced apoptosis. Taken together, our results indicated that ACP induced lysosome-mitochondria mediated apoptosis via H3K27ac-regulated CTSD in HCT-116 cells. This study indicates that ACP has anti-cancer potential in the treatment of colorectal cancer.
Yu WQ, Wang XL, Ji HH, Miao M, Zhang BH, Li H, Zhang ZY, Ji CF, Guo SD CM3-SII polysaccharide obtained from Cordyceps militaris ameliorates hyperlipidemia in heterozygous LDLR-deficient hamsters by modulating gut microbiota and NPC1L1 and PPARalpha levels International Journal of Biological Macromolecules239 (2023)
124293
b-D-Galp-(1-2)-a-D-Manp6Me-(1-4)-+ b-D-Galf-(1-2)-/Variants 0/-+
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-4)-b-D-Manp-(1-6)-b-D-Manp-(1-6)-a-D-Manp-(1-4)-b-D-Manp-(1-6)-b-D-Manp-(1-6)-a-D-Manp-(1-4)-b-D-Manp-(1-
/Variants 0/ is:
b-D-Galp-(1-4)-
OR (exclusively)
b-D-Galf-(1-4)-
NCBI PubMed ID:37011745 Publication DOI:10.1016/j.ijbiomac.2023.124293 Journal NLM ID:7909578 Publisher: Butterworth-Heinemann Correspondence: S.D. Guo < SD-GUOhotmail.com> Institutions: Institute of Lipid Metabolism and Atherosclerosis, Innovative Drug Research Centre, School of Pharmacy, Weifang Medical University, Weifang 261053, China, School of Stomatology, Weifang Medical University, Weifang 261053, China, College of Pharmacy Engineering Research Center for Medicine, Harbin University of Commerce, Harbin 150076, China
Accumulating evidence has demonstrated that polysaccharides derived from edible fungi have lipid-lowering effects in mice. However, the lipid metabolism mechanisms in mice and humans are different. We have previously elucidated the structural characteristics of the alkali-extracted polysaccharide CM3-SII obtained from Cordyceps militaris. This study aimed to investigate whether CM3-SII could ameliorate hyperlipidemia in a heterozygous low-density lipoprotein receptor (LDLR)-deficient hamster model of hyperlipidemia. Our data demonstrated that CM3-SII significantly decreased total plasma cholesterol, non-high-density lipoprotein cholesterol, and triglyceride levels in heterozygous LDLR-deficient hamsters. Unlike ezetimibe, CM3-SII could enhance the concentration of plasma apolipoprotein A1 and the expression of liver X receptor α/ATP-binding cassette transporter G8 mRNA pathway and suppress the expression of Niemann-Pick C1-like 1, which help to reduce cholesterol levels further. Moreover, the results of molecular docking analysis demonstrated that CM3-SII could directly bind to Niemann-Pick C1-like 1 with high affinity. The triglyceride-lowering mechanisms of CM3-SII were related to its downregulation of sterol regulatory element-binding protein 1c and upregulation of peroxisome proliferator-activated receptor α. Importantly, CM3-SII increased the abundance of Actinobacteria and Faecalibaculum and the ratio of Bacteroidetes/Firmicutes. Thus, CM3-SII attenuated hyperlipidemia by modulating the expression of multiple molecules involved in lipid metabolism and the gut microbiota.
Methods: Western blotting, statistical analysis, animal experiments, RT-qPCR, analysis of gut microbiota, alkaline extraction, cell culture Biological activity: In the liver, CM3-SII reduces cholesterol reabsorption and TG synthesis by inhibiting NPC1L1 and SREBP-1c, respectively. Furthermore, this molecule decreases the plasma TG level by enhancing PPARα-mediated fatty acid oxidation. Comments, role: the presumed structure of CM3-SII 3D data: 3D data
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(later renamed to: Cyclocybe cylindracea)
ncu.edu.cn>; S. Nie <spnie