Effecacy of Biejia(Carapax Trionycis) and Ezhu(Rhizoma Curcumae Phaeocaulis) couplet medicine on epithelial-mesenchymal transition, invasion and migration of MDA-MB-231 triple negative breast cancer cells via PI3K/Akt/mTOR signaling pathway

OBJECTIVE:To investigate the efficacy of Biejia(Carapax Trionycis)and Ezhu(Rhizoma Curcumae Phaeocaulis)couplet medicine on epithelial-mesenchymal transition(EMT),invasion and migration of MDA-MB-231 triple negative breast cancer(TNBC)cells based on PI3K/Akt/mTOR signaling pathway.METHODS:MDA-MB-231 cells were treated with different medicated serum as Biejia-,Ezhu-,Biejia-Ezhu(BJ-,EZ-,BJ-EZ-)groups,intervened with no drug rat serum and paclitaxel with final concentration of 33 nM(IC50)as negative and positive control(NC and PC)groups.CCK-8 assay,scratch test,and Transwell assay were used to examine cell proliferation,invasion,and migration.The expression of E-cadherin,N-cadherin,Vimentin,MMP-2,MMP-9,PI3K,Akt,p-Akt,mTOR,and p-mTOR was determined by Western blot,and the m RNA expression of PI3K,Akt and mTOR was determined by real-time polymerase chain reaction.RESULTS:BJ-EZ group inhibited proliferation after 24,48,and 72 h compared with the NC group(P<0.05,<0.01 or<0.001)and reduced the invasion and migration of MDA-MB-231 cells(P<0.01 or<0.001).In addition,BJ-EZ group upregulated the expression of E-cadherin,downregulated the expression of N-cadherin,Vimentin,MMP-2,and MMP-9(P<0.05,P<0.01 or P<0.001),and inhibited the m RNA and protein expression of PI3K,Akt(p-Akt),mTOR(p-mTOR)(P<0.05,<0.01 or<0.001).CONCLUSION:Biejia(Carapax Trionycis)and Ezhu(Rhizoma Curcumae Phaeocaulis)couplet medicine can inhibit the proliferation,invasion,migration and EMT of MDA-MB-231 cells through PI3K/Akt/mTOR signaling pathway,and the effect is better than that of Biejia(Carapax Trionycis)or Ezhu(Rhizoma Curcumae Phaeocaulis)alone.

Optimizing medication strategies for liver cancer:unraveling the mechanisms of key drug combinations in the comprehensive guide to effective tumor prescriptions

This study delved into the formulaic patterns of liver cancer treatment outlined in“The Complete Book of Good Tumor Prescriptions”and explored the action mechanisms of core traditional Chinese medicine(TCM)combinations.Initially,liver cancer treatment formulas were extracted from the aforementioned book,and Excel 2017 was employed for calculating the frequency,properties,and meridians associated with the TCMs.IBM SPSS Modeler 18.0 was utilized for the analysis of TCM association rules,and Cytoscape 3.7.2 was employed for the visualization of these rules.Subsequently,network pharmacology was utilized to analyze the action mechanisms of core TCM combinations,leveraging TCMSP,TCMID,Genecards,DAVID,and other databases.The results revealed the inclusion of 131 prescriptions encompassing 303 TCMs.The core TCMs predominantly comprised those invigorating blood circulation and removing blood stasis,clearing heat,and tonifying deficiencies.The flavor of the TCMs was chiefly bitter or pungent,with a prevailing cold property entering the liver and spleen meridians.Association analysis indicated that the support of Angelicae sinensis radix-Trionycis carapax was the highest.Network pharmacology predictions indicated that Angelicae sinensis radix-Trionycis carapax possessed 20 target genes associated with anti-liver cancer properties,including IL-6,MAPK3,and SRC.Gene survival analysis demonstrated high expression of MAPK3 and SRC in liver cancer patients,correlating with a poor prognosis.KEGG analysis identified major anti-liver cancer pathways for Angelicae sinensis radix-Trionycis carapax,encompassing the cancer pathway,TNF signaling pathway,and prolactin signaling pathway.In summary,this study elucidated that TCMs for liver cancer treatment primarily consisted of invigorating blood circulation and removing blood stasis,antipyretic,and tonifying medicines.The core TCM pair,Angelicae sinensis radix-Trionycis carapax,appeared pivotal in this context.The underlying mechanism might involve the modulation of key genes,such as MAPK3 and SRC,and the regulation of pathways,including the cancer pathway,TNF signaling pathway,and prolactin signaling pathway.