Hepatocellular carcinoma (HCC) is characterized by high metastatic potential and poor prognosis. Ring finger protein 220 (RNF220) has been implicated in tumorigenesis across various cancers; however, its role and associated regulatory mechanisms in HCC remain unclear. In this study, analysis of The Cancer Genome Atlas (TCGA) database revealed that RNF220 expression was significantly elevated in liver hepatocellular carcinoma (LIHC) tissues and was associated with poor prognosis. Further experiments confirmed the upregulation of RNF220 mRNA and protein in HCC tissues. Functional assays demonstrated that RNF220 overexpression promoted cell proliferation, migration and stemness, whereas RNF220 knockdown suppressed these processes in HCC cells. Mechanistically, RNF220 enhanced ubiquitin-specific protease 22 (USP22) expression, leading to activation of the protein kinase B (Akt) pathway. Furthermore, the knockdown of RNF220 inhibited HCC progression, an effect that could be reversed by SC79 (an Akt activator), an Akt activator. In vivo experiments further confirmed that RNF220 aggravated tumor growth and metastasis. In summary, these findings indicate that RNF220 promotes HCC progression by regulating USP22 and activating the Akt pathway, suggesting that RNF220 may serve as a potential biomarker and therapeutic target for HCC.

Hepatocellular carcinoma (HCC) is characterized by high metastatic potential and poor prognosis. Ring finger protein 220 (RNF220) has been implicated in tumorigenesis across various cancers; however, its role and associated regulatory mechanisms in HCC remain unclear. In this study, analysis of The Cancer Genome Atlas (TCGA) database revealed that RNF220 expression was significantly elevated in liver hepatocellular carcinoma (LIHC) tissues and was associated with poor prognosis. Further experiments confirmed the upregulation of RNF220 mRNA and protein in HCC tissues. Functional assays demonstrated that RNF220 overexpression promoted cell proliferation, migration and stemness, whereas RNF220 knockdown suppressed these processes in HCC cells. Mechanistically, RNF220 enhanced ubiquitin-specific protease 22 (USP22) expression, leading to activation of the protein kinase B (Akt) pathway. Furthermore, the knockdown of RNF220 inhibited HCC progression, an effect that could be reversed by SC79 (an Akt activator), an Akt activator. In vivo experiments further confirmed that RNF220 aggravated tumor growth and metastasis. In summary, these findings indicate that RNF220 promotes HCC progression by regulating USP22 and activating the Akt pathway, suggesting that RNF220 may serve as a potential biomarker and therapeutic target for HCC.

Aim: To explore the overall methylation changes in liver tissues during the formation of gallstones, as well as the key pathways and genes involved in the process. Methods: Reduced-representation bisulfite sequencing and RNA sequencing were conducted on the liver tissues of mice with gallstones and control normal mice. Results: A total of 8705 differentially methylated regions in CpG and 1410 differentially expressed genes were identified. The joint analysis indicated that aberrant DNA methylation may be associated with dysregulated gene expression in key pathways such as cholesterol metabolism and bile secretion. Conclusion: We propose for the first time that methylation changes in some key pathway genes in liver tissue may be involved in the formation of gallstones. The methylation status and downstream expression levels of many key pathways involved in gallstones formation were altered in the liver tissue of mice with gallstones. Gallstones are one of the most common gastrointestinal diseases and cause huge medical costs every year around the world. The specific causes of gallstone formation are currently not fully understood. It is not yet known whether DNA methylation is related to the formation of gallstones. This study revealed the overall methylation changes in liver tissue of gallstone mice through reduced-representation bisulfite sequencing and RNA sequencing. A total of 8705 differentially methylated regions in CpG and 1410 differentially expressed genes were identified in the analyzed samples. The methylation status of genes in numerous pathways closely related to gallstone formation, including cholesterol metabolism and bile secretion, was significantly altered. The joint analysis of methylome and transcriptome data indicated that aberrant DNA methylation may be associated with dysregulated gene expression in key pathways such as cholesterol metabolism and bile secretion. In this study, we first proposed that methylation changes in some key pathways in liver tissue may be related to the formation of gallstones. This research result provides a new perspective for understanding the formation mechanism of gallstones.

Aim: To explore the overall methylation changes in liver tissues during the formation of gallstones, as well as the key pathways and genes involved in the process. Methods: Reduced-representation bisulfite sequencing and RNA sequencing were conducted on the liver tissues of mice with gallstones and control normal mice. Results: A total of 8705 differentially methylated regions in CpG and 1410 differentially expressed genes were identified. The joint analysis indicated that aberrant DNA methylation may be associated with dysregulated gene expression in key pathways such as cholesterol metabolism and bile secretion. Conclusion: We propose for the first time that methylation changes in some key pathway genes in liver tissue may be involved in the formation of gallstones. The methylation status and downstream expression levels of many key pathways involved in gallstones formation were altered in the liver tissue of mice with gallstones. Gallstones are one of the most common gastrointestinal diseases and cause huge medical costs every year around the world. The specific causes of gallstone formation are currently not fully understood. It is not yet known whether DNA methylation is related to the formation of gallstones. This study revealed the overall methylation changes in liver tissue of gallstone mice through reduced-representation bisulfite sequencing and RNA sequencing. A total of 8705 differentially methylated regions in CpG and 1410 differentially expressed genes were identified in the analyzed samples. The methylation status of genes in numerous pathways closely related to gallstone formation, including cholesterol metabolism and bile secretion, was significantly altered. The joint analysis of methylome and transcriptome data indicated that aberrant DNA methylation may be associated with dysregulated gene expression in key pathways such as cholesterol metabolism and bile secretion. In this study, we first proposed that methylation changes in some key pathways in liver tissue may be related to the formation of gallstones. This research result provides a new perspective for understanding the formation mechanism of gallstones.

The chemotherapy resistance often leads to chemotherapy failure. This study aims to explore the molecular mechanism by which MUC1 regulates paclitaxel resistance in lung adenocarcinoma (LUAD), providing scientific basis for future target selection. The bioinformatics method was used to analyse the mRNA and protein expression characteristics of MUC1 in LUAD. RT-qPCR and ELISA were used to detect the mRNA and protein expression, flow cytometry was used to detect CD133⁺ cells, and cell viability was detected by CCK-8 assay. The mRNA-seq was performed to analyse the changes in expression profile, GO and KEGG analysis were used to explore the potential biological functions. MUC1 is highly expressed in LUAD patients and is associated with a higher tumour infiltration. In paclitaxel resistance LUAD cells (A549/TAX cells), the expression of MUC1, EGFR/p-EGFR and IL-6 were higher than that of A549 cells, the proportion of CD133⁺ cells was significantly increased, and the expression of cancer stem cell (CSCs) transcription factors (NANOG, OCT4 and SOX2) were significantly up-regulated. After knocking down MUC1 in A549/Tax cells, the activity of A549/Tax cells was significantly decreased. Correspondingly, the expression of EGFR, IL-6, OCT4, NANOG, and SOX2 were significantly down-regulated. The mRNA-seq showed that knocking down MUC1 affected the gene expression, DEGs mainly enriched in NF-κB and MAPK signalling pathway. MUC1 was highly expressed in A549/TAX cells, and MUC1-EGFR crosstalk with IL-6 may be due to the activation of NF-κB and MAPK pathways, which promote the enrichment of CSCs and lead to paclitaxel resistance.

The chemotherapy resistance often leads to chemotherapy failure. This study aims to explore the molecular mechanism by which MUC1 regulates paclitaxel resistance in lung adenocarcinoma (LUAD), providing scientific basis for future target selection. The bioinformatics method was used to analyse the mRNA and protein expression characteristics of MUC1 in LUAD. RT-qPCR and ELISA were used to detect the mRNA and protein expression, flow cytometry was used to detect CD133⁺ cells, and cell viability was detected by CCK-8 assay. The mRNA-seq was performed to analyse the changes in expression profile, GO and KEGG analysis were used to explore the potential biological functions. MUC1 is highly expressed in LUAD patients and is associated with a higher tumour infiltration. In paclitaxel resistance LUAD cells (A549/TAX cells), the expression of MUC1, EGFR/p-EGFR and IL-6 were higher than that of A549 cells, the proportion of CD133⁺ cells was significantly increased, and the expression of cancer stem cell (CSCs) transcription factors (NANOG, OCT4 and SOX2) were significantly up-regulated. After knocking down MUC1 in A549/Tax cells, the activity of A549/Tax cells was significantly decreased. Correspondingly, the expression of EGFR, IL-6, OCT4, NANOG, and SOX2 were significantly down-regulated. The mRNA-seq showed that knocking down MUC1 affected the gene expression, DEGs mainly enriched in NF-κB and MAPK signalling pathway. MUC1 was highly expressed in A549/TAX cells, and MUC1-EGFR crosstalk with IL-6 may be due to the activation of NF-κB and MAPK pathways, which promote the enrichment of CSCs and lead to paclitaxel resistance.

Supplementary figure 1Supplementary tables 1-15

Supplementary figure 1Supplementary tables 1-15

Abstract Anthocyanin/polyvinyl alcohol/chitosan composite membrane was prepared by solution casting method using chitosan (CS) and polyvinyl alcohol (PVA) as matrix and natural pigment anthocyanin as filler. The structures of the composite films were characterized by Uv-visible reflectance spectrum (UV-VIS), Fourier infrared spectroscopy (FT-IR) and the scanning electron microscopy (SEM). The effects of adding anthocyanins on the physical properties, water resistance, degradation, antibacterial properties and pH responsiveness of the films were investigated. The experimental results showed that the prepared anthocyanin/polyvinyl alcohol/chitosan composite indicator films show color changes from pink to purple to blue and then to yellow-green when the pH value ranges from 2 to 14. The total color difference ΔE value is greater than 12. The antibacterial properties and other properties of the composite film can enhance by adding anthocyanin. The tensile strength of anthocyanin/polyvinyl alcohol/chitosan film is more than 70 MPa, which is larger than that of polyvinyl film and polyvinyl alcohol/chitosanfilm. The film has excellent physical, antibacterial properties and obvious pH response performance, making it ideal for food packaging.

Abstract Anthocyanin/polyvinyl alcohol/chitosan composite membrane was prepared by solution casting method using chitosan (CS) and polyvinyl alcohol (PVA) as matrix and natural pigment anthocyanin as filler. The structures of the composite films were characterized by Uv-visible reflectance spectrum (UV-VIS), Fourier infrared spectroscopy (FT-IR) and the scanning electron microscopy (SEM). The effects of adding anthocyanins on the physical properties, water resistance, degradation, antibacterial properties and pH responsiveness of the films were investigated. The experimental results showed that the prepared anthocyanin/polyvinyl alcohol/chitosan composite indicator films show color changes from pink to purple to blue and then to yellow-green when the pH value ranges from 2 to 14. The total color difference ΔE value is greater than 12. The antibacterial properties and other properties of the composite film can enhance by adding anthocyanin. The tensile strength of anthocyanin/polyvinyl alcohol/chitosan film is more than 70 MPa, which is larger than that of polyvinyl film and polyvinyl alcohol/chitosanfilm. The film has excellent physical, antibacterial properties and obvious pH response performance, making it ideal for food packaging.