Background: Honokiol is a major bioactive compound extracted from Magnolia. The present study was designed to determine whether liposomal honokiol has the antitumor activity against human lung cancer as well as potentiates the antitumor activity of cisplatin in A549 lung cancer xenograft model, if so, to examine the possible mechanism in the phenomenon.

Honokiol, a novel antitumor agent, could induce apoptosis and inhibit the growth of vascular endothelium in several tumor cell lines and xenograft models. It has been suggested that the antitumor effect of chemotherapy could be increased by combining it with an antiangiogenesis agent in anticancer strategy. The present study explored the potential to increase the antitumor effect of adriamycin by combining it with honokiol in mouse 4T1 breast cancer models, and the underlining mechanism was investigated. Honokiol was encapsulated in liposomes to improve the water insolubility. In vitro, liposomal honokiol inhibited the proliferation of 4T1 cells via apoptosis and significantly enhanced the apoptosis of 4T1 cells induced by adriamycin. In vivo, the systemic administration of liposomal honokiol and adriamycin significantly decreased tumor growth through increased tumor cell apoptosis compared with either treatment alone. Collectively, these findings suggest that liposomal honokiol may augment the induction of apoptosis in 4T1 cells in vitro and in vivo, and this combined treatment has shown synergistic suppression in tumor progression according to the analysis of isobologram. The present study may be important in future exploration of the potential application of the combined approach in the treatment of breast cancer.

We aimed to investigate the role of the quantitative parameters of dual-energy computed tomography (DECT) in evaluating patients with hepatocellular carcinoma (HCC) treated by transarterial chemoembolization (TACE). We retrospectively identified 80 HCC patients (mean age, 56 years; 61 men) treated by TACE who received contrast-enhanced DECT and were retreated by TACE within 7 days between November 2018 and December 2019. Taking digital subtraction angiography (DSA) and CT images as reference standard, two readers measured and calculated the values of normalized iodine concentration at arterial phase (NICAP), normalized iodine concentration at portal venous phase (NICPP), iodine concentration difference (ICD), arterial iodine fraction (AIF) and slope of the spectral Hounsfield unit curve (λHu) by placing matched regions of interests (ROIs) within the tumor active area (TAA), adjacent normal hepatic parenchyma (ANHP) and tumor necrotic area (TNA). Differences between the parameters were analyzed by the Kruskal–Wallis H test. Receiver operating characteristic analysis of the parameters performance in differentiating the three tissues types was performed. AIF exhibited a good performance in distinguishing TAA (0.93 ± 0.31) and ANHP (0.18 ± 0.14), the areas under the receiver operating characteristic curve (AUC) was 0.989, while the λHu exhibited an excellent performance in distinguishing TAA (3.32 ± 1.24) and TNA (0.29 ± 0.27), with an AUC of 1.000. In conclusion, quantitative DECT can be effectively used to evaluate the tumor viability in HCC patients treated by TACE.

The solubility of 4,4′-dihydroxydiphenyl sulfone in acetonitrile, methanol, ethanol, n-propanol, isopropyl alcohol, acetone, 1-butanol, 2-methyl-1-propanol and ethyl acetate were determined at temperatures from (278.15 to 313.15) K under 101.3 kPa by using a gravimetric method. With the increase in temperature, the solubility of 4,4′-dihydroxydiphenyl sulfone in these solvents increased. The solubility values decreased according to the following order: acetone > acetonitrile > ethyl acetate >1-butanol > (methanol, ethanol, n-propanol, 2-methyl-1-propanol) > isopropyl alcohol. The obtained solubility data were correlated with three models, which corresponded to the modified Apelblat equation, λh equation, and Van't Hoff equation. The evaluated solubility values by the modified Apelblat equation agreed very well with those calculated by the other two models. In general, the regressed results with the three models were all within the acceptable limit for the solubility of 4,4′dihydroxydiphenyl sulfone in the selected solvents. Furthermore, the standard dissolution enthalpies per 1 mol of mixtures of 4,4′-dihydroxydiphenyl sulfone and solvent were evaluated in terms of the modified Apelblat equation. The dissolution process of 4,4′-dihydroxydiphenyl sulfone in these solvents was endothermic. The study concerning the solubility of 4,4′-dihydroxydiphenyl sulfone in the selected solvents and thermodynamic property of dissolution could provide fundamental data in the manufacturing and separating process of 4,4′-dihydroxydiphenyl sulfone.

(1) Background: To assess the efficacy of the quantitative parameters of intravoxel incoherent motion (IVIM) diffusion-weighted imaging for hepatocellular carcinoma (HCC) diagnosis after transarterial chemoembolization (TACE). (2) Methods: Fifty HCC patients after TACE were included and underwent MRI. All of the patients were scanned with the IVIM-DWI sequence and underwent TACE retreatment within 1 week. Referring to digital subtraction angiography (DSA) and MR enhanced images, two readers measured the f, D, and D* values of the tumor active area (TAA), tumor necrotic area (TNA), and adjacent normal hepatic parenchyma (ANHP). Then, the distinctions of the TAA, TNA, and ANHP were compared and we analyzed the differential diagnosis of the parameters in three tissues. (3) Results: For values of f and D, there were significant differences between any of the TAA, TNA, and ANHP (p < 0.05). The values of f and D were the best indicators for identifying the TAA and TNA, with AUC values of 0.959 and 0.955, respectively. The values of f and D performed well for distinguishing TAA from ANHP, with AUC values of 0.835 and 0.753, respectively. (4) Conclusions: Quantitative IVIM-DWI was effective for evaluating tumor viability in HCC patients treated with TACE and may be helpful for non-invasive monitoring of the tumor viability.

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S618proach. Targeting protein kinase Cß (PKCß) may serve as an attractive candidate because activation of PKCß has been implicated in tumor proliferation, survival, invasion, and angiogenesis in model systems. Enzastaurin is a selective PKCß inhibitor. There is evidence for its efficacy in both preclinical and clinical trials. The objective of this study was to assess the effect of enzastaurin on proliferation and phosphoprotein signaling in lung cancer. Methods: Four non small cell lung cancer (non-SCLC) cell lines (H125, H322, H23, A549) and four SCLC cell lines (H69, SW210.5, DMS-79, H211)] were tested. Cells were exposed to different doses of enzastaurin for 4 days, and the anti-proliferation effect was assessed with the CellTiter-Glo Luminescent Cell Viability Assay. The efficiency of enzastaurin in suppressing intracellular phosphoprotein signaling in these cells was tested at 1µmol/L concentrations at difference time points (0.5, 1, 2, 4 hours). PKCβII and phospho-PKCβII(ser660), GSK3β and phospho-GSK3β(ser9), ribosomal protein S6 and phosphoribosomal protein S6(ser240/244) were measured by western blotting. Results: Enzastaurin suppressed cell proliferation of all NSCLC and SCLC cell lines in the low micromolar range (0.1, 1, 5µM). Western blot analysis of these cells showed that phosphorylation of PKCβII(ser660), GSK3β(ser9) and ribosomal protein S6(ser240/244) were suppressed in a time-dependent manner after enzastaurin treatment. Conclusions: These data indicate that enzastaurin has a direct anticancer effect through suppression of proliferation, and they suggest that this effect is mediated by inhibition of intracellular phosphoprotein signaling.