Particle size, polydispersity and zeta potential of liposomes.

<p>The data were expressed as mean±SD (n = 3).</p><p># p <0.05 TSCL-shSATB1 vs. TSCL,TSCL-DOX-shSATB1 vs. TSCL-DOX, TSMCL-shSATB1 vs. TSMCL,TSMCL-DOX-shSATB1 vs. TSMCL-DOX,</p><p>*p <0.05 TSMCL vs. TSCL, TSMCL-DOX vs. TSCL-DOX, TSMCL-shSATB1 vs. TSCL-shSATB1 and TSMCL-DOX-shSATB1 vs. TSCL-DOX-shSATB1.</p

Silencing of SATB1 expression by different liposomes.

<p>(<b>A</b>) Fluorescent imaging of MKN-28 cells transfected by TSCL-shSATB1 and TSMCL-shSATB1. (<b>B</b>) Quantitative analysis of transfection efficiency of TSCL-shSATB1 and TSMCL-shSATB1 by FACS. (<b>C</b>) Western blot analysis of SATB1 protein level in MKN-28 cells transfected by TSCL-shSATB1 and TSMCL-shSATB1. (<b>D</b>) Real-time PCR analysis of SATB1 mRNA level in MKN-28 cells transfected by TSCL-shSATB1 and TSMCL-shSATB1. The values were expressed as mean±SD from three independent experiments. * p<0.05 compared with mock control; # p<0.05 compared with TSCL-shSATB1.</p

DOX release from different liposomes.

<p>The release of DOX from different liposomes at 37°C (<b>A</b>) and 42°C (<b>B</b>) after incubation with PBS or 50% FBS. The values were expressed as mean±SD (n = 3).</p

In vitro anti-tumor effects of different liposomes to MKN-28 cells.

<p>(<b>A</b>) The viability of cells after treatment with liposomes loaded with different concentrations of DOX. (<b>B</b>) The viability of cells after treatment with liposomes loaded with different concentrations of shSATB1. (<b>C</b>) The viability of cells after treatment with liposomes as indicated. The values were expressed as mean±SD (n = 3). (<b>D</b>) The apoptosis of cells after treatment with liposomes as indicated.</p

Uptake of DOX and FAM-labeled siRNA by MKN-28 cells.

<p>(<b>A</b>) Imaging of cells after treatment with TSCL-siRNA and TSMCL-siRNA. (<b>B</b>) Imaging of cells after treatment with TSCL-DOX and TSMCL-DOX. (<b>C</b>) Imaging of cells after treatment with TSCL-DOX-siRNA and TSMCL-DOX-siRNA. (<b>D</b>) Typical detailed imaging of the location of DOX and siRNA in cells after treatment with TSMCL-DOX-siRNA.</p

In vivo anti-tumor activity of different liposomes.

<p>(<b>A</b>) Typical imaging of xenografted tumor. (<b>B</b>) Tumor size after treatment with Free DOX, TSMCL-DOX, TSMCL-shSATB1, TSCL-DOX-shSATB1, or TSMCL- DOX-shSATB1, treatment with normal saline was used as control. Data were presented as mean±SD (n = 6). (<b>C</b>) Survival curves of tumor bearing mice treated with Free DOX, TSMCL-DOX, TSMCL-shSATB1, TSCL-DOX-shSATB1, or TSMCL- DOX-shSATB1, treatment with normal saline was used as control.</p

Prognostic Significance of the Metabolic Marker Hexokinase-2 in Various Solid Tumors: A Meta-Analysis

<div><p>Objective</p><p>Recently, numerous studies have reported that hexokinase-2 (HK2) is aberrantly expressed in cancer, indicating that HK2 plays a pivotal role in the development and progression of cancer. However, its prognostic significance in solid tumor remains unclear. Accordingly, we performed a meta-analysis to assess the prognostic value of HK2 in solid tumor.</p><p>Methods</p><p>Eligible studies were identified using PubMed, Embase, and Web of Science databases. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) for overall survival (OS) or progression-free survival (PFS)/disease-free survival (DFS)/relapse-free survival (RFS) were estimated with random effects or fixed effects models, respectively. Subgroup analysis was also performed according to patients’ ethnicities, tumor types, detection methods, and analysis types.</p><p>Results</p><p>Data from 21 included studies with 2532 patients were summarized. HK2 overexpression was significantly associated with worse OS (pooled HR = 1.90, 95% CI = 1.51–2.38, <i>p</i> < 0.001) and PFS (pooled HR = 2.91, 95% CI = 2.02–4.22, <i>p</i> < 0.001) in solid tumor. As to a specific form of cancer, the negative effect of HK2 on OS was observed in hepatocellular carcinoma (pooled HR = 2.06, 95% CI = 1.67–2.54, <i>p</i> < 0.001), gastric cancer (pooled HR = 1.72, 95% CI = 1.09–2.71, <i>p</i> = 0.020), colorectal cancer (pooled HR = 2.89, 95% CI = 1.62–5.16, <i>p</i> < 0.001), but not in pancreatic cancer (pooled HR = 1.13, 95% CI = 0.28–4.66, <i>p</i> = 0.864). No publication bias was found in the included studies for OS (Begg’s test, <i>p</i> = 0.325; Egger’s test, <i>p</i> = 0.441).</p><p>Conclusion</p><p>In this meta-analysis, we identified that elevated HK2 expression was significantly associated with shorter OS and PFS in patients with solid tumor, but the association varies according to cancer type.</p></div

Funnel plots to evaluate publication bias of included studies for OS.

<p>Funnel plots to evaluate publication bias of included studies for OS.</p

Flow diagram shows search strategy.

<p>Flow diagram shows search strategy.</p

Forest plots to assess the effect of elevated HK2 expression on PFS/DFS/RFS.

<p>Forest plots to assess the effect of elevated HK2 expression on PFS/DFS/RFS.</p