Background: Poria cocos (P. cocos) is an important medicinal fungus in traditional Chinese medicine. Poria acid (PA), a triterpenoid compound, is an effective component of traditional Chinese medicine P. cocos. This experiment investigated the anti-gastric cancer biological activity of PA in vitro. Methods: The effect of PA on the viability of gastric cancer cells was detected by the thiazolyl blue (MTT) assay. Cell adhesion assays were used to detect changes in the adhesion of cells treated after PA (0, 20, 40, and 80 µmol/L). The ability of cell invasion and migration were detected by Transwell assays and wound healing assays. A high-content imaging system was used to dynamically record the motility of the gastric cancer cells after PA (0, 20, 40, and 80 µmol/L) treatment. Western blotting was used to detect the expression of epithelial–mesenchymal transformation (EMT), invasion and migration related proteins. Results: The MTT assay showed that the proliferation of gastric cancer cells was significantly inhibited after PA treatment. Cell adhesion experiments showed that the adhesion of gastric cancer cells was significantly decreased after PA treatment. Compared with the control group, the wound healing area of the gastric cancer cells treated with different concentrations of PA decreased. The Transwell assay showed that the number of gastric cancer cells passing through the cell membrane were significantly reduced after PA treatment. In addition, after PA treatment, the cells’ movement distance and average movement speed were significantly lower than those of the control group. Finally, PA can significantly alter the expression of EMT-related proteins E-cadherin, N-cadherin, and Vimentin and decreased the expressions of metastasis-related proteins matrix metalloproteinase (MMP) 2, MMP-9 and tissue inhibition of matrix metalloproteinase (TIMP)1 in the gastric cancer cells. Conclusions: Triterpenoids from P. cocos have significant biological activity against gastric cancer, and the mechanism may be involved in the process of epithelial–mesenchymal transformation.

Background: Renal cell carcinoma (RCC) is a common cancer of the urinary system. Chinese medicine is being extensively used in the treatment of various cancers. Recent studies found that Poria cocos, a widely used Chinese medicine, has an anti-tumor effect. Pachymic acid (PA) is a triterpenoid compound of P. cocos, and the present study investigated whether PA is a main anti-tumor active ingredient of this fungus. Methods: The effects of PA on cell viability, proliferation, adhesion, invasion, and metastasis were assessed by 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazole bromide, colony formation, cell adhesion, wound healing, and Transwell assays. High-content imaging was used to dynamically observe and verify the inhibitory effect of PA on cell motility, and Western blot was used to detect the expression of matrix metalloproteinase-related proteins and epithelial–mesenchymal transformation proteins. Result: The in vitro assays demonstrated that PA was able to reduce the viability, proliferation, adhesion number, wound healing rate, and transmembrane number of the RCC cells. In addition, high-intensive imaging indicated that PA shortened the traveling distance and slowed the movement of the RCC cells. Western blots showed that in the PA-treated RCC cells, E-cadherin expression was increased, whereas N-cadherin and Vimentin expression was decreased. Furthermore, the expression levels of matrix metalloproteinase-2, matrix metalloproteinase-9, and tissue inhibitor of metalloproteinase-1 were all decreased by the PA administration. Conclusion: PA inhibited the invasion and metastasis of RCC, and these results suggest that PA may be an effective anti-tumor component of P. cocus.

Background Gastric cancer (GC) tumorigenesis and treatment failure are caused by cancer stem cells. Polypyrimidine tract binding protein 1 (PTBP1) was shown to be involved in the development of embryonic stem cells and is now being considered as a therapeutic target for tumour progression and stem-cell characteristics. Methods PTBP1 expression in GC samples was detected using tissue microarrays. Proliferation, colony formation, spheroid formation and stem-cell analysis were used to examine PTBP1’s role in tumorigenesis and stem-cell maintenance. In AGS and HGC-27 cells with or without PTBP1 deficiency, ubiquitin-related protein expression and co-precipitation assays were performed. Results We identified that PTBP1 was aberrantly highly expressed and represented a novel prognostic factor in GC patients. PTBP1 maintained the tumorigenic activity and stem-cell characteristics of GC in vitro and in vivo. PTBP1 directly interacts with c-Myc and stabilises its protein levels by preventing its proteasomal degradation. This is mediated by upregulating the ubiquitin-specific proteases USP28 and limiting FBW7-mediated ubiquitination of c-Myc. Moreover, the depletion of PTBP1-caused tumour regression was significantly compromised by exogenous c-Myc expression. Conclusions By preserving the stability of c-Myc through the ubiquitin–proteasome pathway, the oncogene PTBP1 supports stem-cell-like phenotypes of GC and is involved in GC progression.