T the effect of PEITC was more pronounced in HER2 positive breast cancer cells in vitro and in vivo [32]. Our current study presents a novel role of PEITC in preventing and suppressing 10781694 breast cancer metastasis in vivo possibly by suppressing HER2, EGFR and VEGF, which are known to promote cell motility. Taken together, the results from our study indicate that PEITC suppresses brain metastasis of breast cancer cells.Supporting InformationFigure S1.(EPS)Figure S2.(EPS)AcknowledgmentsKind gift of MDA-MB-231 (BR) cells and HER2 overexpressing MDAMB-231 (HH) cells by Dr. Epigenetic Reader Domain Patricia S. Steeg (National Cancer Institute, Maryland) and Dr. Quentin Smith (Texas Tech University Health Sciences Centre, Amarillo, Texas) are greatly appreciated.Author ContributionsConceived and designed the experiments: PG SKS. Performed the experiments: PG CA. Analyzed the data: PG PL SKS. Contributed reagents/materials/analysis tools: PL SKS. Wrote the paper: PG SKS.
Staphylococcus aureus can cause serious hospital- and communityacquired infections, including skin and soft tissue infections, pneumonia, bacteremia, endocarditis, and even septic shock. The high prevalence of methicillin-resistant S. aureus (MRSA) and the extensive use of vancomycin have led to the emergence of reduced vancomycin susceptibility among S. aureus strains. Heterogeneous vancomycin-intermediate resistant S. aureus (hVISA) [vancomycin minimum inhibitory concentration (MIC) #2 mg/mL], the precursor of vancomycin-intermediate resistant S. aureus (VISA, MIC of 4 2 8 mg/mL), is a strain that contains subpopulations of vancomycin-intermediate daughter cells, but for which the MIC of vancomycin for the parent strain is in the susceptible range. Although vancomycin-resistant S. aureus (VRSA) strains are rare, hVISA/VISA are common in the clinical setting, especially in persistent MRSA bacteremia and endocarditis. Our previous studies have shown that the prevalence of hVISA is 13 to 16 in large teaching hospitals in China [1]. Moreover, several studieshave indicated that hVISA/VISA infections are inhibitor associated with vancomycin treatment failure [2,3]. To date, no specific genetic determinants of hVISA/VISA have been universally defined, whereas VRSA strains acquire the vanA gene from Enterococcus. Several phenotypic features are characteristic of hVISA/VISA strains, among which significant cell wall thickening is a common feature associated with vancomycin resistance [4]. Compared with vancomycin-susceptible S. aureus (VSSA), hVISA produces three to five times the amount of penicillin-binding proteins (PBPs) 2 and 2′. The amounts of intracellular murein monomer precursor in hVISA are three to eight times greater than those in VSSA strains [4]. Factors such as the increased synthesis of non-amidated muropeptides and the resultant reduced peptidoglycan cross-linking contribute to the vancomycin resistance of VISA through increased affinity trapping of vancomycin [5]. In addition to thickened cell walls, hVISA/ VISA strains exhibit other phenotypic changes, including reduction in autolytic activity [6], reduced growth rate [7], resistance to lysostaphin [8], PBP changes [9], and metabolic changes [10].The Comparative Proteomics of hVISASeveral transcriptional changes have been detected in hVISA/ VISA. DNA microarray analyses have been used to determine changes in the transcriptional profile of hVISA or VISA strains [11?5]. However, the protein profiles of hVISA or VISA are rarely analyzed via comparative p.T the effect of PEITC was more pronounced in HER2 positive breast cancer cells in vitro and in vivo [32]. Our current study presents a novel role of PEITC in preventing and suppressing 10781694 breast cancer metastasis in vivo possibly by suppressing HER2, EGFR and VEGF, which are known to promote cell motility. Taken together, the results from our study indicate that PEITC suppresses brain metastasis of breast cancer cells.Supporting InformationFigure S1.(EPS)Figure S2.(EPS)AcknowledgmentsKind gift of MDA-MB-231 (BR) cells and HER2 overexpressing MDAMB-231 (HH) cells by Dr. Patricia S. Steeg (National Cancer Institute, Maryland) and Dr. Quentin Smith (Texas Tech University Health Sciences Centre, Amarillo, Texas) are greatly appreciated.Author ContributionsConceived and designed the experiments: PG SKS. Performed the experiments: PG CA. Analyzed the data: PG PL SKS. Contributed reagents/materials/analysis tools: PL SKS. Wrote the paper: PG SKS.
Staphylococcus aureus can cause serious hospital- and communityacquired infections, including skin and soft tissue infections, pneumonia, bacteremia, endocarditis, and even septic shock. The high prevalence of methicillin-resistant S. aureus (MRSA) and the extensive use of vancomycin have led to the emergence of reduced vancomycin susceptibility among S. aureus strains. Heterogeneous vancomycin-intermediate resistant S. aureus (hVISA) [vancomycin minimum inhibitory concentration (MIC) #2 mg/mL], the precursor of vancomycin-intermediate resistant S. aureus (VISA, MIC of 4 2 8 mg/mL), is a strain that contains subpopulations of vancomycin-intermediate daughter cells, but for which the MIC of vancomycin for the parent strain is in the susceptible range. Although vancomycin-resistant S. aureus (VRSA) strains are rare, hVISA/VISA are common in the clinical setting, especially in persistent MRSA bacteremia and endocarditis. Our previous studies have shown that the prevalence of hVISA is 13 to 16 in large teaching hospitals in China [1]. Moreover, several studieshave indicated that hVISA/VISA infections are associated with vancomycin treatment failure [2,3]. To date, no specific genetic determinants of hVISA/VISA have been universally defined, whereas VRSA strains acquire the vanA gene from Enterococcus. Several phenotypic features are characteristic of hVISA/VISA strains, among which significant cell wall thickening is a common feature associated with vancomycin resistance [4]. Compared with vancomycin-susceptible S. aureus (VSSA), hVISA produces three to five times the amount of penicillin-binding proteins (PBPs) 2 and 2′. The amounts of intracellular murein monomer precursor in hVISA are three to eight times greater than those in VSSA strains [4]. Factors such as the increased synthesis of non-amidated muropeptides and the resultant reduced peptidoglycan cross-linking contribute to the vancomycin resistance of VISA through increased affinity trapping of vancomycin [5]. In addition to thickened cell walls, hVISA/ VISA strains exhibit other phenotypic changes, including reduction in autolytic activity [6], reduced growth rate [7], resistance to lysostaphin [8], PBP changes [9], and metabolic changes [10].The Comparative Proteomics of hVISASeveral transcriptional changes have been detected in hVISA/ VISA. DNA microarray analyses have been used to determine changes in the transcriptional profile of hVISA or VISA strains [11?5]. However, the protein profiles of hVISA or VISA are rarely analyzed via comparative p.