Shaolin Li

Preparation and characterization of baicalin-poly -vinylpyrrolidone coprecipitate.

Baicalin-polyvinylpyrrolidone (PVP) coprecipitate was prepared by the solvent method of solid dispersion technology to improve the dissolution rate of baicalin. The coprecipitate was characterized using differential scanning calorimetry (DSC), X-ray powder diffraction (XRD), infrared spectrometry (IR) and dissolution testing. Furthermore, AFM·IPC-208B high-resolution atomic force microscopy (AFM) was utilized to characterize the molecular morphology of baicalin within its carrier and the interaction between baicalin and its carrier. The results of DSC and XRD indicated that baicalin resided in PVP polymers in an amorphous or molecular phase, dissolution test results demonstrated that the dissolution rate of the coprecipitate was 21.4 times that of the active pharmaceutical ingredient (API). The results of IR indicated the possibility of the formation of intermolecular hydrogen bonds. The AFM·IPC-208B findings revealed that baicalin was dispersed in PVP polymers with a molecular size of 2 nm and either wrapped or surrounded by approximately 0.4 nm of a five-membered ring of PVP arranged along the carbon chain sequentially. An intermolecular hydrogen bond was formed between the 4-OH of the glucuronide of baicalin and the O of the carbonyl group from PVP in addition to the formation of intramolecular hydrogen bonds within baicalin.

(-)-Epigallocatechin-3-gallate inhibits nasopharyngeal cancer stem cell self-renewal and migration and reverses the epithelial–mesenchymal transition via NF-κB p65 inactivation

The cancer stem cell (CSC) theory states that many types of cancer, including nasopharyngeal cancer (NPC), are initiated from and maintained by CSCs, which may be responsible for tumor relapse and resistance to therapy. It is imperative that nasopharyngeal cancer stem cells (NPCSCs) be specifically targeted to eradicate NPC and prevent recurrence. Epigallocatechin-3-gallate (EGCG) inhibits cancer progression by attenuating NF-κB p65 activity, which is upregulated in CSCs and plays an important role in epithelial–mesenchymal transition (EMT). The purpose of this study is to confirm the self-renewal and migration inhibitory effects of EGCG toward NPCSCs and to clarify its mechanism of activity. We enriched and characterized NPCSCs by collecting spheroid-derived cells grown in serum-free medium (SFM) and examined the effects of EGCG on the characteristics of NPCSCs and studied the underlying mechanisms using soft agar colony assays, transwell migration assays, reverse transcriptase polymerase chain reaction (RT-PCR), Western blot analysis, immunofluorescence staining, and xenograft studies. NPC spheroids enriched from NPC cell lines acquired CSC traits and underwent EMT. EGCG inhibited the NPCSCs’ self-renewal and migration and reversed EMT, and combined treatment with EGCG and cisplatin reduced the growth of CSC tumor xenografts. Moreover, EGCG inhibited NF-κB p65 activity by modulating the cellular localization of p65 and decreasing the transcriptional regulation of NF-κB p65 on Twist1 expression. NF-κB p65 is a novel therapeutic target in NPCSCs, and the inhibition of activated NF-κB p65 in CSCs by EGCG may offer an effective treatment for NPC.

IL-6/STAT3/TWIST inhibition reverses ionizing radiation-induced EMT and radioresistance in esophageal squamous carcinoma

The acquisition of radioresistance by esophageal squamous carcinoma (ESC) cells during radiotherapy may lead to cancer recurrence and poor survival. Previous studies have demonstrated that ionizing radiation (IR) induces epithelial–mesenchymal transition (EMT) of ESC cells accompanied by increased migration, invasion, and radioresistance. However, the underlying molecular mechanisms of IR-induced EMT and radioresistance are not well established, hampering the development of potential solutions. To address this issue, we investigated the role of the IL-6/STAT3/TWIST signaling pathway in IR-induced EMT. We found not only the pathway was activated during IR-induced EMT but also STAT3 inhibition or Twist depletion reversed the EMT process and attenuated radioresistance. These results improve our understanding of the underlying mechanisms involved in IR-induced EMT and suggest potential interventions to prevent EMT-induced acquisition of radioresistance.

Dissolution and pharmacokinetics of baicalin–polyvinylpyrrolidone coprecipitate

Baicalin–polyvinylpyrrolidone coprecipitate was prepared with the aim of improving the dissolution and bioavailability of the baicalin.

Identification of biomarkers for hepatocellular carcinoma using network-based bioinformatics methods

BackgroundHepatocellular carcinoma (HCC) is one of the most common types of cancer worldwide. Despite several efforts to elucidate molecular mechanisms involved in this cancer, they are still not fully understood.MethodsTo acquire further insights into the molecular mechanisms of HCC, and to identify biomarkers for early diagnosis of HCC, we downloaded the gene expression profile on HCC with non-cancerous liver controls from the Gene Expression Omnibus (GEO) and analyzed these data using a combined bioinformatics approach.ResultsThe dysregulated pathways and protein-protein interaction (PPI) network, including hub nodes that distinguished HCCs from non-cancerous liver controls, were identified. In total, 29 phenotype-related differentially expressed genes were included in the PPI network. Hierarchical clustering showed that the gene expression profile of these 29 genes was able to differentiate HCC samples from non-cancerous liver samples. Among these genes, CDC2 (Cell division control protein 2 homolo g), MMP 2 (matrix metalloproteinase-2) and DCN (Decorin were the hub nodes in the PPI network.ConclusionsThis study provides a portfolio of targets useful for future investigation. However, experimental studies should be conducted to verify our findings.

Association Between TGF-β1 Polymorphisms and Hepatocellular Carcinoma Risk: A Meta-Analysis

BACKGROUND Associations between transforming growth factor (TGF)-β1 polymorphisms and hepatocellular carcinoma (HCC) risk remained controversial. Therefore, we performed this meta-analysis to investigate these associations. METHODS We searched Pubmed, EMBASE, Chinese National Knowledge Infrastructure (CNKI), and Wanfang databases for studies before March 2013. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to calculate the strength of association. RESULTS A total of 14 studies were included in this meta-analysis. TGF-β1 +869C/T polymorphism was significantly associated with HCC risk (OR=1.74, 95% CI: 1.22-2.47, p=0.002). In addition, a significant association between -509C/T polymorphism and HCC risk was observed (OR=1.40, 95% CI: 1.15-1.70, p=0.0007). Furthermore, significant associations between these polymorphisms and HCC risk were found in Asians and population-based studies. CONCLUSIONS Our meta-analysis suggested that the TGF-β1 +869C/T and -509C/T polymorphisms may be risk factors for developing HCC.