Acetylated nanocellulose reinforced hydroxypropyl starch acetate realizing polypropylene replacement for green packaging application.

The use of natural starch as a replacement for petroleum-based packaging materials is limited due to its poor processability, weak mechanical properties, and strong moisture sensitivity. To address these limitations, this study adopts molecular design of hydroxypropylation and acetylation to sequentially modify natural starch, and material design of introducing acetylated cellulose nanofibers (ACNF) into the starch matrix to reinforce the material. Hydroxypropylation decreased the interaction force between the starch molecular chains, thereby reducing the glass transition temperature. Subsequent acetylation introduced hydrophobic acetyl groups that disrupted intermolecular hydrogen bonds, enhancing the mobility of the starch molecular chain, and endowed the hydroxypropyl starch acetate (HPSA) with excellent thermoplastic processability (melt index of 7.12 g/10 min) without the need for plasticizers and notable water resistance (water absorption rate of 3.0 %). The introduction of ACNF generated a strong interaction between HPSA chains, promoting the derived ACNF-HPSA to exhibit excellent mechanical strength, such as high impact strength of 2.1 kJ/m2, tensile strength of 22.89 MPa, elasticity modulus of 813.22 MPa, flexural strength of 24.18 MPa and flexural modulus of 1367.88 MPa. Its overall performance even surpassed that of polypropylene (PP) plastic, making it a potential alternative material for PP-based packaging materials.

Corneodesmosin as a potential target of oral squamous cell carcinoma.

OBJECTIVE: The relationship between oral squamous cell carcinoma (OSCC) and Corneodesmosin (CDSN) remains unclear. This study aims to explore the correlation between CDSN and the prognosis and survival time of patients with OSCC. METHODS: Bioinformatics were used to identify the hub role of CDSN in the OSCC. A total of 200 patients with OSCC were recruited. Clinical and follow-up data were recorded, and the expression level of CDSN was detected. Pearson chi-square test and Spearman correlation coefficient were used to analyze the relationship between prognosis and related parameters in patients with OSCC. Univariate and multivariate Logistic regression and Cox proportional risk regression were applied for further analysis, and receiver operating characteristic curve and survival curve of subjects were plotted. RESULTS: CDSN was identified as the most significant hub gene of the OSCC by the cytoHubba. By the comparative toxicogenomics database (CTD) analysis, there was strong relationship between the CDSN and mouth neoplasms, head and neck neoplasms, squamous cell carcinoma of head and neck. The OSCC patients with low expression level of CDSN have poor overall survival compared with the high expression level of CDSN (HR = 0.75, 95% confidence interval [95%CI]: 0.57-0.98, P = .036). Spearman correlation coefficient analysis showed that CDSN expression level was significantly correlated with prognosis (ρ = -0.528, P < .001). Multivariate Logistic regression analysis showed that poor prognosis (odds ratio [OR] = 0.096, 95%CI: 0.049-0.189, P < .001) was significantly associated with low expression of CDSN. Cox regression analysis showed that the survival time of OSCC patients was shorter when CDSN expression was low (HR = 0.588, 95%CI: 0.420-0.823, P = .002). Strong predictive value of CDSN for the OSCC survival time was obtained by the biological process (BP)-neural network and support vector machine (SVM). CONCLUSION: CDSN was significantly correlated with OSCC, and the shorter the survival time of patients with OSCC was, the worse the prognosis was.

COL11A1 as a potential prognostic target for oral squamous cell carcinoma.

Oral squamous cell carcinoma (OSCC) is a malignant tumor occurring in the oral cavity. However, the molecular mechanism of OSCC is not clear. Bioinformatics was used to screen and identify role of collagen type X1 alpha 1 (COL11A1) on OSCC. 200 patients with OSCC were recruited. Clinical and follow-up data were recorded and COL11A1 expression levels were tested. Pearson chi-square test and Spearman correlation coefficient were used to analyze relationship between prognosis and related parameters in patients with OSCC. Univariate and multivariate Logistic regression, univariate and multivariate Cox proportional risk regression were used for further analysis, survival curve was drawn. Through bioinformatics analysis, OSCC patients with higher expression of COL11A1 have poor overall survival compare with OSCC patients with lower expression of COL11A1 (hazard ratios [HR] = 1.32, P = .047). Pearson chi-square test showed that age (P = .011), tumor grade (P = .023), COL11A1 (P < .001) was significantly correlated with prognosis of OSCC. Univariate Logistic regression analysis showed age (odds ratio [OR] = 2.102, 95% confidence intervals [95%CI]: 1.180-3.746, P = .012), tumor grade (OR = 1.919, 95%CI: 1.093-3.372, P = .023) and COL11A1 (OR = 12.775, 95%CI: 6.509-25.071, P < .001). Multivariate Logistic regression analysis showed that COL11A1 (OR = 12.066, 95%CI: 6.042-24.096, P < .001) was significantly associated with prognosis of patients with OSCC. Univariate Cox regression analysis showed that age (HR = 1.592, 95%CI: 1.150-2.205, P = .005), tumor grade (HR = 1.460, 95%CI: 1.067-1.999, P = .018) and COL11A1 (HR = 1.848, 95%CI: 1.340-2.548, P < .001) were significantly correlated with survival time of OSCC patients. Multivariate Cox regression analysis showed that tumor grade (HR = 1.466, 95%CI: 1.064-2.020, P = .019) and COL11A1 (HR = 1.645, 95%CI: 1.164-2.325, P = .005) were significantly correlated with survival time of OSCC patients. COL11A1 is significantly correlated with occurrence of OSCC. When COL11A1 is highly expressed, prognosis of patients with OSCC is worse and the survival time is shorter.

MKI67 an potential oncogene of oral squamous cell carcinoma via the high throughput technology.

Oral squamous cell carcinoma is a malignant tumor that occurs in the oral cavity, with poor prognosis and easy recurrence. However, the relationship between MKI67 and oral squamous cell carcinoma remains unclear. The oral squamous cell carcinoma datasets GSE138206, GSE146483 and GSE184616 were downloaded from the gene expression omnibus database, and the differentially expressed genes (DEGs) were screened. The protein-protein interaction network was constructed and analyzed by search tool for the retrieval of interacting genes database and Cytoscape software. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) were used for functional enrichment analysis. GO and KEGG analyses were performed on the whole genome, as formulated by gene set enrichment analysis. comparative toxicogenomics database was used to identify the diseases most associated with the core genes. TargetScan was used to screen miRNA regulating central DEGs. A total of 1472 DEGs were identified. GO analysis showed that the differentially expressed genes were mainly enriched in the tissues of extracellular matrix, type i interferon signaling pathway, human papillomavirus infection, adhesion spot, hepatitis C and ECM-receptor interaction. Enrichment items were similar to GO and KEGG enrichment items of differentially expressed genes. 10 core genes were obtained, and their expression was different between oral squamous cell carcinoma and normal tissue samples. MKI67 is highly expressed in oral squamous cell carcinoma and may be an oncogene in oral squamous cell carcinoma.

The POLR2E rs3787016 polymorphism is associated with susceptibility to and prognosis of gastric cancer.

Long non-coding RNAs (lncRNAs) have been proposed as promising diagnostic and prognostic biomarkers for cancer. We investigated the associations of RNA polymerase II subunit E (POLR2E) rs3787016 polymorphism with the risk and prognosis of gastric cancer (GC). The study subjects included 368 GC patients who underwent surgical resection and 294 healthy volunteers, adjusted for age, gender, smoking status, alcohol status, and Helicobacter pylori infection status. The data was subjected to logistic regression analyses and revealed that the subjects carrying AA genotype of rs3787016 in POLR2E had a significant 1.85-1.98-fold increased risk of GC when compared with those carrying GG genotype (adjusted OR=1.979, 95% CI=1.198-3.267; p=0.008) or those carrying AG/GG genotypes (adjusted OR=1.847, 95% CI=1.222-2.793; p=0.004). For the GC patients, the AA genotype of rs3787016 was significantly correlated with poorly differentiated GC (p=0.018), advanced TNM stage (p=0.023), higher depth of invasion (p=0.022), positive lymph node metastasis (p=0.01), and worse overall survival (OS; p=0.004). Multivariate analysis confirmed that the POLR2E rs3787016 polymorphism is an independent prognostic factor for GC (HR=1.668, 95% CI=1.058-2.631; p=0.028). Our cumulative results thus suggest that the presence of POLR2E rs3787016 polymorphism could serve as a genetic factor that affects the susceptibility to and the prognosis of GC.

HSPA9 overexpression inhibits apoptin-induced apoptosis in the HepG2 cell line.

Apoptin, a small protein derived from chicken anemia virus, possesses the capacity to specifically kill tumor cells while leaving normal cells intact. Previous studies have indicated that the subcellular localization of apoptin appears to be crucial for this tumor-selective activity. Apoptin resides in the cytoplasm of normal cells; however, in cancer cells it translocates into the nucleus. In the present study, purified prokaryotic native His-apoptin served as a bait for capturing apoptin-associated proteins in both a hepatoma carcinoma cell line (HepG2) and a human fetal liver cell line (L-02). The captured proteins obtained from a pull-down assay were separated by two-dimensional gel electrophoresis. Mass spectrometry was employed to detect the effect of HSPA9 overexpression (one of the interacting proteins with apoptin in vitro) and downregulation of HSPA9 on HepG2 cells. The data revealed that HSPA9 overexpression resulted in partial distribution of apoptin in the cytoplasm. Notably, HSPA9 overexpression markedly decreased the apoptosis rate of HepG2 cells from 41.2 to 31.7%, while the downregulation of HSPA9 using small interfering RNA significantly enhanced the apoptosis of HepG2 cells. Our results suggest new insights into the localization mechanism of apoptin which is tightly associated with HSPA9 overexpression and its crucial role in cellular apoptosis both in a tumor cell line (HepG2) and a normal cell line (L-02). These findings shed new light on the elucidation of the underlying mechanism of anticancer action of apoptin.

PTD4-apoptin protein and dacarbazine show a synergistic antitumor effect on B16-F1 melanoma in vitro and in vivo.

PTD4-apoptin protein enters cells and harbors tumor-selective cell death activity. Dacarbazine is the mainstay of treatment for malignant melanoma. In this study, we investigated the cytotoxic effect of PTD4-apoptin protein and/or dacarbazine in mouse B16-F1 and human A875 and SK-MEL-5 melanoma cells in vitro and by means of a mouse B16-F1 melanoma model in vivo. PTD4-apoptin protein inhibits the growth of B16-F1, A875 and SK-MEL-5 melanoma cells in a dose-dependent manner, but not in normal human cell lines WI-38 and L-02. PTD4-apoptin combined with dacarbazine revealed a synergistic cytotoxic effect (coefficient of drug interaction<1) in all three different tumor cell lines. In vivo, PTD4-apoptin protein and dacarbazine alone effectively inhibited the growth of B16-F1 melanoma in C57BL/6 mice. Strikingly, combined PTD4-apoptin/dacarbazine treatment significantly increased the antitumor effect in comparison to the single treatments. As important, a combined PTD4-apoptin/dacarbazine treatment with a 50% reduction of dacarbazine revealed similar antitumor activities, without detectable hematologic side effects. A combined PTD4-apoptin/dacarbazine treatment represents a promising novel efficient and safe anticancer strategy.

TFPI or uPA-PAI-1 complex affect cell function through expression variation of type II very low density lipoprotein receptor.

Very low density lipoprotein receptors (VLDLR) including type I and type II are known to affect cell functions by binding to its extracellular ligands. However, the effect of these ligands on VLDLR expression remains elusive. Tissue factor pathway inhibitor (TFPI) and urokinase plasminogen activator and plasminogen activator inhibitor 1 (uPA-PAI-1) complex, two ligands of VLDLR, were used to examine their effects on VLDLR expression. TFPI treatment decreased type II VLDLR expression, inhibited cell proliferation and migration, and degradated beta-catenin in SGC7901 cells. However, uPA-PAI-1 complex, increased type II VLDLR expression with promoted cell proliferation and migration and stabilization of beta-catenin. These results indicated that extracellular ligands can change the expression of type II VLDLR to affect cell proliferation and migration.

Construction of a fusion protein expression vector MK-EGFP and its subcellular localization in different carcinoma cell lines.

AIM: To construct an expression plasmid encoding human wild-type midkine (MK) and enhanced green fluorescence protein (EGFP) fusion protein (MK-EGFP), and to analyze the subcellular localization of MK in different carcinoma cell lines. METHODS: Two kinds of MK coding sequences with or without signal peptide were cloned into plasmid pEGFP-N2, and the recombinant plasmids constructed were introduced into HepG2, MCF7 and DU145 cells, respectively, by transfection. With the help of laser scanning confocal microscopy, the expression and subcellular localization of MK-GFP fusion protein could be detected. RESULTS: Compared with the GFP control, in which fluorescence was detected diffusely over the entire cell body except in the nucleolus, both kinds of fusion protein MK-GFP were localized exclusively to the nucleus and accumulated in the nucleolus in the three kinds of cancer cell lines. CONCLUSION: This study reveals the specific nucleolar translocation independent of signal peptide, which may be involved in the mechanism that MK works. It provides valuable evidence for further study on the functions of MK in nucleus and its possible mechanisms, in which ribosomal RNA transcription and ribosome assembly are involved.