In this study, isoliquiritigenin (ISL) incorporated nanoliposomes were prepared and their effects on colorectal cancer (CRC) cell lines were investigated. Herein, we sought to explore the anti-cancer mechanisms of ISL loaded nanoliposomes (ISL-NLs) on AMP-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) pathways mediated glycolysis. Also, the key targets such as caveolin 1 (CAV1), glucose transporters and Akt/mTOR that promote glycolysis, and are activated via the induction of α-enolase (ENO1), fructose bisphosphate aldolase A (ALDOA) and monocarboxylate transporter 4 (MCT4) expressions were also investigated. It was shown that ISL-NLs significantly suppressed the proliferation and glucose uptake of CRC cell by potentially regulating the glycolysis and lactate targets as well as pathways that formed the basis of the anti-CRC effects of ISL-NLs. The mechanism underlying this effect was further validated via the regulation of some key targets such as ENO1, ALDOA, lactate dehydrogenase A (LDHA) and MCT4 in glycolysis coupled with cellular myelocytomatosis oncogene (c-myc), hypoxia-inducible factor 1-alpha (HIF-1α) in protein kinase B/mTOR (Akt/mTOR) pathways. Moreover, the AMPK proteins were identified to be up-regulated while the lactic acid production was suppressed by ISL-NLs in the CRC cells, indicating that ISL-NLs had an inhibitory effect on AMPK mediated glycolysis and lactate production. Altogether, these results have provided insights into the mechanism underlying the key role that liposomal ISL played in the multiple inhibition of AMPK and Akt/mTOR mediated glycolysis and lactate generation, which may be regulated as the alternative metabolic pathways of CRC as well as serve as adjuvant therapy for the disease.

Objective. To investigate the relationship between polymorphism of FOXA1 gene rs12894364 and rs7144658 and susceptibility to gastric cancer. Methods. A case-control study was conducted to select 577 cases of primary gastric cancer and 678 cases of normal control. We extracted whole blood genomic DNA and amplified the target gene fragment by PCR. The genotyping and allele was tested through a snapshot method. Results. There was no significant difference in the frequency distribution of genotype between the case group and control group ( ). Stratified analyses showed the SNPs were not correlated with the susceptibility of GC according to different age, gender, cigarette smoking, and alcohol drinking status. Conclusion. There is no significant correlation between the polymorphisms of FOXA1 gene rs12894364 and rs7144658 and the risk of gastric cancer.

Objective. To investigate the relationship between polymorphism of TNFRSF11 gene rs9533156 and rs2277438 and susceptibility to gastric cancer. Methods. A case-control study was conducted to select 577 cases of primary gastric cancer and 678 cases of normal control. We extracted whole blood genomic DNA and amplified the target gene fragment by PCR. The genotyping and allele were tested through the snapshot method. Results. In this case-control study, we observed that there was a difference in the genotype distribution of TNFRSF11 gene rs9533156 between the case group and the control group. The frequency distribution of TC heterozygous mutation in the case group was higher than that in the control group. The smoking rate in the case group (34.49%) was higher than that in the control group (27.29%), and the difference in frequency distribution between the two groups was statistically significant (P=0.006). Our findings suggest that TNFRSF11 rs9533156 is associated with susceptibility to GC, which is more evident among elderly patients (>62 years), nonsmokers, and patients who do not consume alcohol. The analysis of the relationship between the TNFSF11 gene rs9533156 site variant and clinical factors of gastric cancer showed that, compared with the tumor size <2 cm group, patients with tumor size ≥2 cm and whom carrying rs9533156 site mutations had a higher frequency distribution, and the difference was statistically significant (P=0.022). Compared with the nonhyperglycemic group, the frequency distribution of patients with rs9533156 site mutations in the diabetes group was higher, and the difference was statistically significant (P<0.001). Conclusion. This study shows that there is a correlation between smoking and the occurrence of gastric cancer. Based on our research, the functional SNP TNFRSF11 TC genotype may be an indicator of individual susceptibility to GC. The mutation at rs9533156 may be related to the size of gastric cancer. The mutation rate of rs9533156 of TNFSF11 gene is higher in diabetic gastric cancer patients.

This case sought to manage a duodenal fistula patient who underwent an open abdomen with vacuum-assisted temporary abdominal closure (VAC) by evaluating his tolerance to early enteral nutrition therapy (ENT). A review of the patient suggested that he developed an abdominal infection as a result of a high duodenal fistula, which necessitated an open abdomen and VAC. Prior to the initiation of ENT, the patient had a patient-generated subjective global assessment (PG-SGA) score of 8 (1st day) suggesting the need for nutritional intervention. Upon ENT intervention, the patient's PG-SGA score dropped to 2 (30th day) indicating an improvement in the nutritional status, probably due to measures such as formulation, implementation, and management of early ENT. The improved nutritional status of the patient led to the success of duodenal fistula repair and abdominal wall defect reconstruction within a short time, thus ensuring a successful surgery.

Introduction: Kushenol E is a prenylated flavonoid derived from Sophora flavescens. Although preliminary studies have suggested that Kushenol E possesses anticancer activity, its effects and molecular mechanisms in Colorectal Cancer (CRC) remain largely unexplored. Therefore, this study investigated the therapeutical effects of Kushenol E and its underlying molecular mechanisms against CRC. Methods: HT-29 cells, colorectal organoids, and an AOM/DSS-induced colorectal tumor model in mice were used. Cellular biomarkers related to growth, damage, programmed cell death, mitochondrial membrane integrity, and activation of the p38, ERK, and AKT signal cascades were measured. In vivo, survival rate, body weight, disease activity index, colon length, tumor volume, H&E staining, TUNEL assays, immunohistochemistry, and ELISA were assessed. Results: Kushenol E inhibited HT-29 cell proliferation, induced apoptosis, increased the expression of mitochondrial apoptosis-related proteins Bax and Caspase-3, and reduced Bcl-2 expression. Kushenol E also reduced phospho-ERK and phospho-AKT levels while increasing phospho-p38. In CRC organoids, Kushenol E significantly reduced organoid diameter on day 3 (p < 0.01) and decreased organoid viability (p < 0.01). In AOM/DSS-treated mice, Kushenol E showed increased TUNEL positivity and Bax and caspase-3 expression, together with reduced Ki67 and PCNA expression. Moreover, ELISA analysis showed that Kushenol E reduced serum levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and lowered the tumorassociated biomarker CEA. Discussion: Kushenol E inhibited CRC cell and organoid growth and attenuated AOM/DSSinduced colorectal tumorigenesis. These effects are associated with mitochondrial apoptosis and alterations in p38/ERK/AKT signaling, and are accompanied by reduced inflammatory cytokine and CEA levels in vivo. Conclusion: Kushenol E has shown excellent antitumor activity against CRC and warrants further mechanistic, pharmacological, and safety evaluation.