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6 results on '"Renbin Shen"'

1. Designing a microbial fermentation-functionalized alginate microsphere for targeted release of 5-ASA using nano dietary fiber carrier for inflammatory bowel disease treatment

Author

Lei Qiu, Renbin Shen, Lei Wei, Shujuan Xu, Wei Xia, Yan Hou, Jinxin Cui, Rong Qu, Jiale Luo, Jian Cao, Jie Yang, Jing Sun, Ronglin Ma, and Qiang Yu

Subjects
Nano dietary fibers, Colitis targeting, Gut microbiota, 5-ASA, Gel microspheres, Biotechnology, TP248.13-248.65, Medical technology, R855-855.5
Abstract

Abstract Patients with inflammatory bowel disease (IBD) always suffer from severe abdominal pain and appear to be at high risk for colorectal cancer. Recently, the co-delivery of targeted drugs and gut microbiota has developed into an attractive strategy. A new strategy using gut microbiota fermentation to overcome the interspace diffuse resistance from the mucus layer to control drug release in inflammatory bowel sites (IBS sites) has not yet been available. Here, we designed an alginate hydrogel microsphere encapsulating bifidobacterium (Bac) and drug-modified nanoscale dietary fibers (NDFs). The hydrogel microsphere is responsible for protecting drugs from acidic and multi-enzymatic environments and delivering drugs to the colorectum. Subsequently, the fermentation of Bac by digesting NDFs and proteins as carbon and nitrogen sources can promote drug release and play a probiotic role in the gut microbiota. In vitro evidence indicated that small-sized NDF (NDF-1) could significantly promote short-chain fatty acid (SCFA) expression. Notably, NDF-1 hydrogel microspheres showed a boost release of 5-ASA in the IBS sites, resulting in the amelioration of gut inflammation and remodeling of gut microbiota in chronic colitis mice. This study developed a controlled release system based on microbial fermentation for the treatment of IBD.

Published
2023
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2. The crosstalk between anoikis and epithelial-mesenchymal transition and their synergistic roles in predicting prognosis in colon adenocarcinoma

Author

Jiahui Zhou, Sheng Yang, Dawei Zhu, Hao Li, Xinsheng Miao, Menghui Gu, Wei Xu, Yan Zhang, Wei Tang, Renbin Shen, Jianhua Zha, Jianhua Zhu, Zheng Yuan, and Xinhua Gu

Subjects
colon adenocarcinoma, anoikis, EMT, crosstalk, risk model, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Anoikis and epithelial-mesenchymal transition (EMT) are significant phenomena occurring in distant metastasis of colon adenocarcinoma (COAD). A comprehensive understanding of their crosstalk and the identification of key genes are vital for treating the distant metastasis of COAD. The objective of this study was to design and validate accurate prognostic predictors for COAD patients based on the anoikis and EMT processes. We obtained gene signatures from various databases and performed univariate and multivariate Cox regression analyses, principal component analysis (PCA). The COAD patients were categorized into the worst prognosis group, the Anoikis Potential Index (API) Low + EMT Potential Index (EPI) High group and the others group. Then we utilized gene set enrichment analysis (GSEA) to identify differentially expressed genes and to establish a prognostic risk model. The model classified patients into high- or low-risk groups, with patients in the high-risk group displaying worse survival status. A nomogram was established to predict overall survival rates, demonstrating high specificity and sensitivity. Additionally, we connected the risk model to the tumor microenvironment (TME) using single-sample GSEA and the MCP counter tool, as well as evaluated the sensitivity to common chemotherapeutic drugs, such as Gefitinib and Gemcitabine. Lastly, cell and tissue experiments suggested a positive correlation among anoikis resistance, EMT, and liver/lung metastasis of COAD. This is the first study to comprehensively analyze the crosstalk between anoikis and EMT and offers new therapeutic targets for COAD metastasis patients.

Published
2023
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3. Fbxo21 regulates the epithelial-to-mesenchymal transition through ubiquitination of Nr2f2 in gastric cancer

Author

Weifeng Qian, Xinyu Liu, Renbin Shen, Yannan Jiang, and Xinhua Gu

Subjects
0301 basic medicine, proliferation, Vimentin, 03 medical and health sciences, 0302 clinical medicine, Immune system, Ubiquitin, medicine, Epithelial–mesenchymal transition, Nr2f2, Gene knockdown, biology, Chemistry, gastric cancer, EMT, Cancer, medicine.disease, Ubiquitin ligase, 030104 developmental biology, Oncology, Cell culture, 030220 oncology & carcinogenesis, embryonic structures, biology.protein, Cancer research, Fbxo21, Research Paper
Abstract

F-box protein 21 (Fbxo21), a member of the F-box family proteins, constitutes one of the four subunits of an E3 ubiquitin ligase complex called SCFs (SKP1-Cullin-F-box). Despite the effect on antivirus immune response and ubiquitination regulation of a few oncoproteins, such as EID1 and P-gp, little is known about the Fbxo21 function in tumors, including gastric cancer. In our study, we confirmed that Fbxo21 expression was decreased in gastric cancer tissues. Decreased expression of Fbxo21 was significantly associated with poor prognosis in gastric cancer. Fbxo21 inhibited gastric cancer progression by inducing growth arrest and inhibiting migration and invasion. The expression of various EMT markers, such as E-cadherin, N-cadherin and Vimentin were altered after Fbxo21 knockdown or overexpression. Moreover, we demonstrated that Fbxo21 inhibited the EMT via the down-regulation of Nr2f2. Fbxo21 expression was negatively correlated with Nr2f2 protein expression in gastric cancer tissues and cell lines. And the Nr2f2 protein abundance was regulated by Fbxo21 via ubiquitination and proteasomal degradation. At last, we demonstrated the effects of Nr2f2 re-expression and inhibition on stable Fbxo21-overexpression or Fbxo21-silenced cell lines. These results suggested that Fbxo21 inhibited the proliferation and EMT in part through down-regulating the Nr2f2.

Published
2021

4. Identification of biomarkers predicting the chemotherapeutic outcomes of capecitabine and oxaliplatin in patients with gastric cancer

Author

Menghui Gu, Renbin Shen, Xinhua Gu, Zhen Yuan, Yan Zhang, Wei Xu, and Yannan Jiang

Subjects
0301 basic medicine, Oncology, Cancer Research, medicine.medical_specialty, medicine.medical_treatment, capecitabine and oxaliplatin, chemotherapy, Capecitabine, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Chemotherapy, Oncogene, business.industry, gastric cancer, capecitabine, oxaliplatin, Area under the curve, biomarkers, Articles, Molecular medicine, Oxaliplatin, Regimen, 030104 developmental biology, 030220 oncology & carcinogenesis, business, Adjuvant, medicine.drug
Abstract

The capecitabine and oxaliplatin (CapeOX) regimen is a commonly used adjuvant chemotherapeutic regimen for gastric cancer (GC). However, some patients exhibit a poor chemotherapy response due to genetic differences among individuals. Therefore, finding an effective sensitization strategy for CapeOX is important in the treatment of GC. The present study aimed to investigate the predictive biomarkers of the CapeOX chemotherapeutic outcomes for patients with GC. A total of 30 differentially expressed genes (DEGs) were identified using the gene expression profiles from The Cancer Genome Atlas capecitabine and oxaliplatin treatment GC cases and seven key DEGs [uroplakin-1b (UPK1B), fatty acid-binding protein, heart (FABP3), cystatin-M, caspase-5 (CASP5), corticosteroid 11-β-dehydrogenase isozyme 2, cytochrome P450 4X1 (CYP4X1) and epidermal growth factor receptor kinase substrate 8-like protein 3] were associated with survival. Gene validation was performed in clinical samples divided into recurrence and nonrecurrence groups. Patients with high or low expression of UPK1B, FABP3, CASP5 and CYP4X1 had markedly different overall survival rates. A model was established and the area under the curve of the receiver operating characteristic reached 0.875 (0.793-0.957), indicating that the model had good sensitivity and specificity.

Published
2020

5. Inhibition of Splicing Factor 3b Subunit 1 (SF3B1) Reduced Cell Proliferation, Induced Apoptosis and Resulted in Cell Cycle Arrest by Regulating Homeobox A10 (HOXA10) Splicing in AGS and MKN28 Human Gastric Cancer Cells

Author

Yannan Jiang, Zhen Yuan, Renbin Shen, Yan Zhang, Wei Xu, Xinhua Gu, and Menghui Gu

Subjects
Spliceosome, Cell Survival, Splicing Factor 3B Subunit 1, Apoptosis, 030204 cardiovascular system & hematology, snRNP Core Proteins, 03 medical and health sciences, Exon, 0302 clinical medicine, Lab/In Vitro Research, Stomach Neoplasms, Cell Line, Tumor, medicine, Humans, RNA, Messenger, Cell Proliferation, Gene knockdown, Cell growth, Chemistry, Alternative splicing, Genes, Homeobox, Cell Cycle Checkpoints, Exons, General Medicine, Phosphoproteins, Cell biology, Gene Expression Regulation, Neoplastic, Alternative Splicing, Cell nucleus, Homeobox A10 Proteins, medicine.anatomical_structure, 030220 oncology & carcinogenesis, RNA splicing, Epoxy Compounds, RNA, Long Noncoding, Macrolides, RNA Splicing Factors
Abstract

BACKGROUND Small nuclear ribonucleoproteins (snRNPs) complexes of protein and noncoding RNA accumulate in the cell nucleus and catalyze pre-mRNA splicing to form the spliceosome. This study aimed to investigate the role of the spliceosome, splicing factor 3b subunit 1 (SF3B1), in AGS and MKN28 human gastric cancer cells in vitro, including gene knockdown with small interfering RNA (siRNA), and the use of the selective mRNA splicing inhibitor of SF3B1, pladienolide B. MATERIAL AND METHODS In AGS and MKN28 human gastric cancer cells, SF3B1expression was inhibited with siRNA and pladienolide B. Following SF3B1 inhibition, the Cell Counting Kit-8 (CCK-8) assay measured cell proliferation, and flow cytometry was used to investigate cell apoptosis and cell cycle arrest. The downstream HOXA10 and AKT pathways were studied by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot. The presence of alternative splicing, or differential splicing, of single-gene coding for multiple proteins, was analyzed using The Cancer Genome Atlas (TCGA) SpliceSeq. RESULTS Inhibition of SF3B1 reduced the proliferation rate of AGS and MKN28 human gastric cancer cells by inducing apoptosis and G2/M phase arrest. SF3B1 knockdown resulted in reduced homeobox A10 (HOXA10) mRNA expression and expression of long noncoding RNA (lncRNA) isoforms of HOXA10 (exons 1 and 3) and HOXA10 (exons 2 and 3). SF3B1 inhibition increased PTEN levels and reduced AKT protein phosphorylation. CONCLUSIONS In AGS and MKN28 human gastric cancer cells in vitro, inhibition of SF3B1 reduced cell proliferation, induced apoptosis, and resulted in cell cycle arrest by regulating HOXA10 splicing.

Published
2020

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