Ziyang Sun, Siqi Zhang, Lei Zhao, Shuhao Wang, Zhen-dong Lin, A. Jin
Ferroptosis has been shown to be a non-self apoptotic, iron ion-catalysed, controlled cell death process involving cellular lipid oxides. The gnes that may affect ferroptosis may be candidate biomarkers. But the value and predictive value of ferroptosis-related genes in colorectal adenocarcinoma (COAD) are not fully understood. Therefore, we analyzed the expression status in COAD and healthy colon tissue using GEO, GEPIA and HPA databases. The role of predictive and genetic alterations of ferroptosis-related genes were investigated using cBioPortal, HPA, PrognoScan, STRING, GeneMANIA and LinkedOmics databases. Then, immunohistochemistry staining was performed to detect the both epithelial and stromal expression of FTL in COAD. Using FerrDb and GEO databases, the transcript levels of XBP1, TSC22D3 and YWHAE were identified to correlate with advanced tumor stage, FTL, DUSP1, TSC22D3 and GDF15 were related to poor prognosis of COAD. As immunohistochemistry staining shown that FTL was significantly up-regulated in COAD tissues. Cox survival analysis and KM survival analysis indicated that high epithelial FTL levels is associated with a poor prognosis in COAD.
{"title":"Identification of Epithelial FTL Expression as an Important Predictor for Prognosis of Colon Adenocarcinoma","authors":"Ziyang Sun, Siqi Zhang, Lei Zhao, Shuhao Wang, Zhen-dong Lin, A. Jin","doi":"10.1166/jbt.2023.3275","DOIUrl":"https://doi.org/10.1166/jbt.2023.3275","url":null,"abstract":"Ferroptosis has been shown to be a non-self apoptotic, iron ion-catalysed, controlled cell death process involving cellular lipid oxides. The gnes that may affect ferroptosis may be candidate biomarkers. But the value and predictive value of ferroptosis-related genes in colorectal adenocarcinoma\u0000 (COAD) are not fully understood. Therefore, we analyzed the expression status in COAD and healthy colon tissue using GEO, GEPIA and HPA databases. The role of predictive and genetic alterations of ferroptosis-related genes were investigated using cBioPortal, HPA, PrognoScan, STRING, GeneMANIA\u0000 and LinkedOmics databases. Then, immunohistochemistry staining was performed to detect the both epithelial and stromal expression of FTL in COAD. Using FerrDb and GEO databases, the transcript levels of XBP1, TSC22D3 and YWHAE were identified to correlate with advanced\u0000 tumor stage, FTL, DUSP1, TSC22D3 and GDF15 were related to poor prognosis of COAD. As immunohistochemistry staining shown that FTL was significantly up-regulated in COAD tissues. Cox survival analysis and KM survival analysis indicated that high epithelial FTL levels\u0000 is associated with a poor prognosis in COAD.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43891859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: Purpose of this work was to discuss effects and mechanisms of Sema 4C in colon cancer development. Results: Sema4C were significantly upregulated in cancer tissues (P <0.001). Following transfection, the expression levels of Sema4C mRNA were significantly downregulated in the si-Sema4C groups compared with those in the si-negative control groups of both HT-29 and SW620 cells (both P <0.001). The apoptotic rate was significantly increased, while the invasive and wound healing rates were significantly suppressed in the si-Sema4C groups of HT-29 and SW620 cells (both P < 0.001). The results of the RT-qPCR and western blotting analyses revealed that PI3K, AKT, MMP-2 and MMP-9 mRNA and protein expression levels, respectively, were significantly downregulated, while caspase-3 mRNA and protein expression levels were significantly upregulated in the si-Sema4C groups of HT-29 and SW620 cells. Conclusion: The findings of the present study demonstrated that the knockdown of Sema4C expression suppressed CRC cell biological activities by regulating the PI3K/AKT signaling pathway. Therefore, Sema4C may act as an oncogene in CRC.
{"title":"Semaphorin 4C Plays a Key Role in Colorectal Cancer Cells Development","authors":"Hongyue Lin, Yuzhu Wu, Jinping Chen, Shurong Huang, Yang Zeng, Wei Zheng","doi":"10.1166/jbt.2023.3264","DOIUrl":"https://doi.org/10.1166/jbt.2023.3264","url":null,"abstract":"Objective: Purpose of this work was to discuss effects and mechanisms of Sema 4C in colon cancer development. Results: Sema4C were significantly upregulated in cancer tissues (P <0.001). Following transfection, the expression levels of Sema4C mRNA were significantly\u0000 downregulated in the si-Sema4C groups compared with those in the si-negative control groups of both HT-29 and SW620 cells (both P <0.001). The apoptotic rate was significantly increased, while the invasive and wound healing rates were significantly suppressed in the si-Sema4C groups\u0000 of HT-29 and SW620 cells (both P < 0.001). The results of the RT-qPCR and western blotting analyses revealed that PI3K, AKT, MMP-2 and MMP-9 mRNA and protein expression levels, respectively, were significantly downregulated, while caspase-3 mRNA and protein expression levels were\u0000 significantly upregulated in the si-Sema4C groups of HT-29 and SW620 cells. Conclusion: The findings of the present study demonstrated that the knockdown of Sema4C expression suppressed CRC cell biological activities by regulating the PI3K/AKT signaling pathway. Therefore, Sema4C may\u0000 act as an oncogene in CRC.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43014107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To discuss sealing properties between BeeFill 2in1 warm vertical compaction technique and cold lateral compaction technique. Methods: Group1 BeeFill 2in1, Group 2: cold lateral compaction. The leakage specimens were measured using the transverse root sectioning, after 1 month. Results: The statistical analysis showed that the frequency of section with void, the percentage of void area and the percentage of sections at 1 mm–13 mm levels, the BeeFill 2in1 group were lower than those of the cold lateral compaction group. Conclusion: BeeFill 2in1 warm vertical compaction technique has its advantage in dealing with the long oval canal.
{"title":"Sealing Efficiency of BeeFill 2in1 Filling Technique and Cold Lateral Compaction Technique","authors":"Ning Zhang, Jiuyu Ge","doi":"10.1166/jbt.2023.3231","DOIUrl":"https://doi.org/10.1166/jbt.2023.3231","url":null,"abstract":"Objective: To discuss sealing properties between BeeFill 2in1 warm vertical compaction technique and cold lateral compaction technique. Methods: Group1 BeeFill 2in1, Group 2: cold lateral compaction. The leakage specimens were measured using the transverse root sectioning,\u0000 after 1 month. Results: The statistical analysis showed that the frequency of section with void, the percentage of void area and the percentage of sections at 1 mm–13 mm levels, the BeeFill 2in1 group were lower than those of the cold lateral compaction group. Conclusion:\u0000 BeeFill 2in1 warm vertical compaction technique has its advantage in dealing with the long oval canal.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47933752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Guangming Luo, Zhangshun Yao, Yan Yang, Jiachuan Chai, Lilin Fu
Purpose: Previous studies have demonstrated the osteogenic effects of icariside II (ICSII), which is a metabolic product of the prenylated active flavonol icariin (ICA) from the roots of Epimedium. However, the in vivo osteogenic effects of ICSII remain unclear. Thus, in this study, we evaluated the osteogenic effects of ICSII in vivo. Methods: Complexes of calcium phosphate cement (CPC) and bone marrow mesenchymal stem cells (BMSCs) with or without ICSII were subcutaneously implanted into nude mice (ectopic osteogenesis test) and into tooth sockets in beagles after maxillary canine tooth extraction (in situ osteogenesis test). The samples were harvested at different time points, and the in vivo osteogenic effect of the ICSII on the BMSCs was evaluated by histology, microcomputed tomography (micro-CT) and the bone mineralization apposition rate (MAR). Results: The proliferation and viability of BMSCs in the ICSII-loaded CPC scaffold were significantly increased (P < 0.01). The new bone area and MAR in the CPC+BMSC+ICSII group were greater than those in the CPC+BMSC group (P < 0.05), but there was no significant difference in markers evaluated by immunohistochemistry and integrated optical density (IOD) analysis (P > 0.05), with the exception of Runx-2 expression in the CPC+BMSC+ICSII group. After 2 months, the bone mineral content (BMC) and specific bone surface (bone surface divided by bone volume, BS/BV) were significantly increased (P < 0.05) in the CPC+BMSC+ICSII group compared with the CPC+BMSC group. The bone mineral density (BMD), bone volume divided by total volume (BV/TV), and trabecular number (Tb.N) were increased in the CPC+BMSC+ICSII group, but the differences were not significant (P > 0.05). Conclusions: Our results suggest that ICSII can likely induce bone formation by BMSCs and be used as a promising factor for building scaffold composites in bone tissue engineering.
{"title":"Icariside II-Loaded Calcium Phosphate Cement Scaffolds Combined with Bone Marrow Mesenchymal Stem Cells for Osteogenesis","authors":"Guangming Luo, Zhangshun Yao, Yan Yang, Jiachuan Chai, Lilin Fu","doi":"10.1166/jbt.2023.3268","DOIUrl":"https://doi.org/10.1166/jbt.2023.3268","url":null,"abstract":"Purpose: Previous studies have demonstrated the osteogenic effects of icariside II (ICSII), which is a metabolic product of the prenylated active flavonol icariin (ICA) from the roots of Epimedium. However, the in vivo osteogenic effects of ICSII remain unclear. Thus,\u0000 in this study, we evaluated the osteogenic effects of ICSII in vivo. Methods: Complexes of calcium phosphate cement (CPC) and bone marrow mesenchymal stem cells (BMSCs) with or without ICSII were subcutaneously implanted into nude mice (ectopic osteogenesis test) and into tooth\u0000 sockets in beagles after maxillary canine tooth extraction (in situ osteogenesis test). The samples were harvested at different time points, and the in vivo osteogenic effect of the ICSII on the BMSCs was evaluated by histology, microcomputed tomography (micro-CT) and the bone\u0000 mineralization apposition rate (MAR). Results: The proliferation and viability of BMSCs in the ICSII-loaded CPC scaffold were significantly increased (P < 0.01). The new bone area and MAR in the CPC+BMSC+ICSII group were greater than those in the CPC+BMSC group (P <\u0000 0.05), but there was no significant difference in markers evaluated by immunohistochemistry and integrated optical density (IOD) analysis (P > 0.05), with the exception of Runx-2 expression in the CPC+BMSC+ICSII group. After 2 months, the bone mineral content (BMC) and specific bone\u0000 surface (bone surface divided by bone volume, BS/BV) were significantly increased (P < 0.05) in the CPC+BMSC+ICSII group compared with the CPC+BMSC group. The bone mineral density (BMD), bone volume divided by total volume (BV/TV), and trabecular number (Tb.N) were increased in the\u0000 CPC+BMSC+ICSII group, but the differences were not significant (P > 0.05). Conclusions: Our results suggest that ICSII can likely induce bone formation by BMSCs and be used as a promising factor for building scaffold composites in bone tissue engineering.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45735147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yifan Mao, Feiyun Jiang, Rui Xu, Fanglei Yang, Yuan Li, Li Li
Introduction: To explore the pathogenesis of gestational diabetic nephropathy (GDM) and its possible biological function by using large data bioinformatics mining algorithm. Materials and methods: The Gene Expression Omnibus (GEO) was retrieved and the data of GDM differential expression chip were screened and downloaded. The differentially expressed genes were screened by using R software Lima package (Log2FC > 1; P < 0.05). Functional enrichment of differentially expressed genes was performed. Protein–protein interaction network of GDM pathogenesis was constructed by the database (STRING) to analyze the interaction between differentially expressed gene-coding proteins. Using Cytohubb software to further screen the key genes (hub genes) in the signaling pathway. In next step, 35 case of GDM and 39 normal pregnant women were selected as subjects. The expression levels of key gene coding proteins in venous blood and placenta tissues of GDM and normal pregnant women detected by immunohistochemical and qRT-PCR. And using cell experiment to analysis the key gene’s effects in GDM. Results: By Bioinformatics Analysis, CDK1 was significantly depressed in GDM (P <0.001), In clinical data, CDK1 protein and mRNA expressions were also significantly down-regulation in GDM compared with NC (P <0.001). In vitro study, with high glucose treatment, the cell were hyperproliferation with CDK1 depressing and AKT overexpression (P <0.001). However, with CDK1 supplement, the cell returned to normal with CDK1 overexpression and AKT depressing (P <0.001). Conclusion: CDK1 is differentially expressed in patients with GDM and play a key part in occurrence and development of GDM. CDK1 may be a key target for treatment and prevention of GDM.
{"title":"CDK1 in Pathogenesis of Gestational Diabetes Mellitus: A Bioinformatics Analysis and Verification","authors":"Yifan Mao, Feiyun Jiang, Rui Xu, Fanglei Yang, Yuan Li, Li Li","doi":"10.1166/jbt.2023.3272","DOIUrl":"https://doi.org/10.1166/jbt.2023.3272","url":null,"abstract":"Introduction: To explore the pathogenesis of gestational diabetic nephropathy (GDM) and its possible biological function by using large data bioinformatics mining algorithm. Materials and methods: The Gene Expression Omnibus (GEO) was retrieved and the data of GDM differential\u0000 expression chip were screened and downloaded. The differentially expressed genes were screened by using R software Lima package (Log2FC > 1; P < 0.05). Functional enrichment of differentially expressed genes was performed. Protein–protein interaction network of GDM pathogenesis\u0000 was constructed by the database (STRING) to analyze the interaction between differentially expressed gene-coding proteins. Using Cytohubb software to further screen the key genes (hub genes) in the signaling pathway. In next step, 35 case of GDM and 39 normal pregnant women were selected as\u0000 subjects. The expression levels of key gene coding proteins in venous blood and placenta tissues of GDM and normal pregnant women detected by immunohistochemical and qRT-PCR. And using cell experiment to analysis the key gene’s effects in GDM. Results: By Bioinformatics Analysis,\u0000 CDK1 was significantly depressed in GDM (P <0.001), In clinical data, CDK1 protein and mRNA expressions were also significantly down-regulation in GDM compared with NC (P <0.001). In vitro study, with high glucose treatment, the cell were hyperproliferation with\u0000 CDK1 depressing and AKT overexpression (P <0.001). However, with CDK1 supplement, the cell returned to normal with CDK1 overexpression and AKT depressing (P <0.001). Conclusion: CDK1 is differentially expressed in patients with GDM and play a key part in occurrence\u0000 and development of GDM. CDK1 may be a key target for treatment and prevention of GDM.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43567492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MiR-608 is expressed in bladder cancer, colon cancer, prostate cancer risk, and exerts inhibitory role in gastric cancer and invasion of three negative malignant breast cancer by inhibiting the NIFC, but its role in the biology of glioma is unclear, so the purpose of this study was to explore MiR-608’s role in glioma, and further explore whether NFIC signal pathways are involved in the role of MiR-608 in glioma. We obtain glioma tissues and normal tissues to detect the expression of miR-608 by PCR. miR-608 mimics transfection or joint with NFIC expression plasmid were transfected into A172, and LN229 glioma cells followed by analysis of cell proliferation, clone formation, invasion and migration, and cell apoptosis. Compared to normal tissue, miR-608 expression in glioma tissues was decreased. After transfection of miR-608 mimics, miR-608 level, cell proliferation activity, invasion and migration activity increased significantly, and apoptosis reduced, in addition, the dual luciferase report gene and protein imprinting analysis showed NFIC to be a target of miR-608. NFIC transfection reversed miR-608’s role in glioma cells. In conclusion, microRNA-608 inhibits malignant invasion and migration of glioma cells via NFIC signaling.
{"title":"MicroRNA-608 Regulates Epithelial-To-Mesenchymal Transition to Inhibit Malignant Behaviors of Glioma Cells Through Nuclear Factor I-C Signaling Pathway","authors":"Yuning Ma, Jing Cao, Tao Fan","doi":"10.1166/jbt.2023.3273","DOIUrl":"https://doi.org/10.1166/jbt.2023.3273","url":null,"abstract":"MiR-608 is expressed in bladder cancer, colon cancer, prostate cancer risk, and exerts inhibitory role in gastric cancer and invasion of three negative malignant breast cancer by inhibiting the NIFC, but its role in the biology of glioma is unclear, so the purpose of this study was\u0000 to explore MiR-608’s role in glioma, and further explore whether NFIC signal pathways are involved in the role of MiR-608 in glioma. We obtain glioma tissues and normal tissues to detect the expression of miR-608 by PCR. miR-608 mimics transfection or joint with NFIC expression plasmid\u0000 were transfected into A172, and LN229 glioma cells followed by analysis of cell proliferation, clone formation, invasion and migration, and cell apoptosis. Compared to normal tissue, miR-608 expression in glioma tissues was decreased. After transfection of miR-608 mimics, miR-608 level, cell\u0000 proliferation activity, invasion and migration activity increased significantly, and apoptosis reduced, in addition, the dual luciferase report gene and protein imprinting analysis showed NFIC to be a target of miR-608. NFIC transfection reversed miR-608’s role in glioma cells. In conclusion,\u0000 microRNA-608 inhibits malignant invasion and migration of glioma cells via NFIC signaling.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41576697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Glial cell line derived neurotrophic factor (GDNF) is a potent neurotrophic factor, which has been shown to affect the metastasis and invasion of cancer cells. The molecular mechanism of GDNF is still unclear. Here, we investigate the mechanism of GDNF embedded in chitosan (CS) nano lipid carrier in colorectal cancer. Methods: Electron microscopy was used to detect the relationship between the characteristics of GDNF chitosan (CS) coated nano lipid carrier, MTT and apoptosis tests were used to detect the effect of GDNF chitosan nano lipid carrier expression on the proliferation ability of intestinal cancer cells, and immunofluorescence was used to detect the effect of GDNF chitosan nano lipid carrier expression on NF-KB signal. The results were verified by western-blot. In vivo using a mouse model. Results: GDNF chitosan nano lipid carrier showed positive zeta value, indicating that the process of CS coating GDNF was successful. OD values of nanocomposites at different concentrations were measured by UV spectrophotometer with MTT. Our data showed that the experimental group showed a relationship between concentration and dose dependent on tolerance growth, indicating that GDNF chitosan nano lipid carrier had better anti-tumor activity in colorectal cancer cell lines. Compared with most GDNF chitosan nano lipid carrier groups, the expression of NF-κB immunofluorescence detection signal was inhibited, and the expression of NF-κB was down-regulated in colorectal cancer. In vivo results showed that the measured tumor volume decreased after treatment with GDNF chitosan nanoparticle lipid carrier, and the survival of mice treated with GDNF chitosan nanoparticle lipid carrier was longer. Conclusion: GDNF chitosan nano lipid carrier can inhibit the expression of NF-κB signal and reduce the proliferation of tumor In vivo, thus slowing down the occurrence and development of intestinal cancer cells.
{"title":"Glial Cell Line-Derived Neurotrophic Factor Chitosan Nanolipid Carrier Inhibits Intestinal Carcinoma via Restraining NF-κB Activity","authors":"Liangrun Zhu, Qi-sheng Jiang, Jun Fang, Gang Bian","doi":"10.1166/jbt.2023.3262","DOIUrl":"https://doi.org/10.1166/jbt.2023.3262","url":null,"abstract":"Background: Glial cell line derived neurotrophic factor (GDNF) is a potent neurotrophic factor, which has been shown to affect the metastasis and invasion of cancer cells. The molecular mechanism of GDNF is still unclear. Here, we investigate the mechanism of GDNF embedded in\u0000 chitosan (CS) nano lipid carrier in colorectal cancer. Methods: Electron microscopy was used to detect the relationship between the characteristics of GDNF chitosan (CS) coated nano lipid carrier, MTT and apoptosis tests were used to detect the effect of GDNF chitosan nano lipid carrier\u0000 expression on the proliferation ability of intestinal cancer cells, and immunofluorescence was used to detect the effect of GDNF chitosan nano lipid carrier expression on NF-KB signal. The results were verified by western-blot. In vivo using a mouse model. Results: GDNF chitosan\u0000 nano lipid carrier showed positive zeta value, indicating that the process of CS coating GDNF was successful. OD values of nanocomposites at different concentrations were measured by UV spectrophotometer with MTT. Our data showed that the experimental group showed a relationship between concentration\u0000 and dose dependent on tolerance growth, indicating that GDNF chitosan nano lipid carrier had better anti-tumor activity in colorectal cancer cell lines. Compared with most GDNF chitosan nano lipid carrier groups, the expression of NF-κB immunofluorescence detection signal was\u0000 inhibited, and the expression of NF-κB was down-regulated in colorectal cancer. In vivo results showed that the measured tumor volume decreased after treatment with GDNF chitosan nanoparticle lipid carrier, and the survival of mice treated with GDNF chitosan nanoparticle\u0000 lipid carrier was longer. Conclusion: GDNF chitosan nano lipid carrier can inhibit the expression of NF-κB signal and reduce the proliferation of tumor In vivo, thus slowing down the occurrence and development of intestinal cancer cells.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46038357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Mahmoud, Omar A. Albaradie, Abdulaziz M. Moglan, Fayhan J. Alroqi, A. Alkayyal
Oncolytic viruses (OVs) are engineered to replicate selectively within cancer cells and destroy them while also inducing an immune response against the virus and the tumor. The Maraba MG1 strain is a double mutant of the Maraba virus that preferentially targets and kills cancer cells while minimizing harm to normal cells through interferon-dependent mechanisms. In preclinical tumor models, MG1 has demonstrated potent antitumor effects. Here, we demonstrate the feasibility of using synthetic DNA genome technology to engineer MG1 to develop a biosimilar oncolytic virus by modifying one of its commonly used restriction enzyme sites for an easy one-step cloning process. The ability to precisely modify the genome sequence of the virus allows greater control over its properties, and the simplified process of gene insertion accelerates the development of new therapies. Our platform will support the translation of this virus as a cancer treatment and provide a streamlined platform for personalized MG1 immunotherapy.
{"title":"Reconstruction of the Oncolytic Maraba MG1 Virus from a Fully Synthetic DNA Genome","authors":"A. Mahmoud, Omar A. Albaradie, Abdulaziz M. Moglan, Fayhan J. Alroqi, A. Alkayyal","doi":"10.1166/jbt.2023.3276","DOIUrl":"https://doi.org/10.1166/jbt.2023.3276","url":null,"abstract":"Oncolytic viruses (OVs) are engineered to replicate selectively within cancer cells and destroy them while also inducing an immune response against the virus and the tumor. The Maraba MG1 strain is a double mutant of the Maraba virus that preferentially targets and kills cancer cells\u0000 while minimizing harm to normal cells through interferon-dependent mechanisms. In preclinical tumor models, MG1 has demonstrated potent antitumor effects. Here, we demonstrate the feasibility of using synthetic DNA genome technology to engineer MG1 to develop a biosimilar oncolytic virus by\u0000 modifying one of its commonly used restriction enzyme sites for an easy one-step cloning process. The ability to precisely modify the genome sequence of the virus allows greater control over its properties, and the simplified process of gene insertion accelerates the development of new therapies.\u0000 Our platform will support the translation of this virus as a cancer treatment and provide a streamlined platform for personalized MG1 immunotherapy.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45320280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study sought for investigating the function of miR-184 in resistance of gastric cancer (GC) cells to cisplatin (DDP). Consequently, not only BGC-823 DDP-resistant GC cells (BGC-823/DDP) but also SGC-7901 DDP-resistant cells (SGC-7901/DDP) were upregulated in contrast with their parent cells. Ectopic expressed miR-184 mimetics increased DDP resistance and increased migration as well as invasion in cisplatin-resistant cells. Nevertheless, miR-184 inhibitors reduced DDP resistance, cell invasion as well as migration in parent cells. Besides, Ncor2 is a direct targeting gene for miR-184 in GC cells. Ncor2 gene knockout revealed that DDP resistance promoted cisplatin-resistant cells. Conversely, over Ncor2 expression in BGC-823 cells generated the effect of suppressing resistance to cisplatin. Additionally, over miR-184 expression raised the resistance of cisplatin-resistant cells to DDP, in part arise from the activation of the Ncor2/PI3K/AKT/mTOR signal pathway. miR-184 could also lessen the sensitivity of BGC-823/DDP cells to cisplatin in vivo. To conclude, we evidence that the inactivation of miR-184 or the activation of channel of its target gene can be served as an innovation to reverse DDP resistance in GC.
{"title":"MicroRNA-184 Increases the Resistance of Gastric Cancer to Cisplatin via PI3K/AKT/mTOR","authors":"S. Ding, Keli Zhong, Kaibin Huang, Ligang Xia","doi":"10.1166/jbt.2023.2624","DOIUrl":"https://doi.org/10.1166/jbt.2023.2624","url":null,"abstract":"This study sought for investigating the function of miR-184 in resistance of gastric cancer (GC) cells to cisplatin (DDP). Consequently, not only BGC-823 DDP-resistant GC cells (BGC-823/DDP) but also SGC-7901 DDP-resistant cells (SGC-7901/DDP) were upregulated in contrast with their\u0000 parent cells. Ectopic expressed miR-184 mimetics increased DDP resistance and increased migration as well as invasion in cisplatin-resistant cells. Nevertheless, miR-184 inhibitors reduced DDP resistance, cell invasion as well as migration in parent cells. Besides, Ncor2 is a direct targeting\u0000 gene for miR-184 in GC cells. Ncor2 gene knockout revealed that DDP resistance promoted cisplatin-resistant cells. Conversely, over Ncor2 expression in BGC-823 cells generated the effect of suppressing resistance to cisplatin. Additionally, over miR-184 expression raised the resistance of\u0000 cisplatin-resistant cells to DDP, in part arise from the activation of the Ncor2/PI3K/AKT/mTOR signal pathway. miR-184 could also lessen the sensitivity of BGC-823/DDP cells to cisplatin in vivo. To conclude, we evidence that the inactivation of miR-184 or the activation of channel\u0000 of its target gene can be served as an innovation to reverse DDP resistance in GC.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47406907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Non-Hodgkin’s lymphoma (NHL) is one highly heterogeneous tumor originating from the lymphatic system. Its morbidity rate shows a gradually increasing trend year by year. The present study determined that the possible function and mechanisms of EIF3D on cell proliferation of NHL. A total of 24 patients with NHL were obtained at Aerospace Center Hospital. In patients with NHL, mRNA and protein expression of EIF3D was up-regulated. Patients with low EIF3D possessed better survival rate. EIF3D stimulated cell proliferation and the number of Edu cells through the activation of Warburg effect in vitro model of NHLNHL. Sh-EIF3D diminished NHL cell proliferation and the number of Edu cells through the inactivation of Warburg effect in vitro model of NHL. Then, we found that EIF3D reduced GRP78 protein ubiquitination to induce GRP78/Akt proteins, and si-EIF3D promote GRP78 protein ubiquitination to suppress GRP78/Akt proteins in vitro model of NHL. Our results indicate that EIF3D promote NHL cell proliferation throughWarburg effect by the inhibition of GRP78 protein ubiquitination, suggesting that it may prove to be one clinical target and pre-tumor gene for NHL.
{"title":"Eukaryotic Translation Initiation Factor 3 Subunit D is One Clinical Target and Pre-Tumor Gene for Non Hodgkin Lymphoma to Promote Cell Proliferation Through Warburg Effect by Interacting with GRP78","authors":"Zhong Kong, Yong Liu, Jing Zhu","doi":"10.1166/jbt.2023.3261","DOIUrl":"https://doi.org/10.1166/jbt.2023.3261","url":null,"abstract":"Non-Hodgkin’s lymphoma (NHL) is one highly heterogeneous tumor originating from the lymphatic system. Its morbidity rate shows a gradually increasing trend year by year. The present study determined that the possible function and mechanisms of EIF3D on cell proliferation of NHL.\u0000 A total of 24 patients with NHL were obtained at Aerospace Center Hospital. In patients with NHL, mRNA and protein expression of EIF3D was up-regulated. Patients with low EIF3D possessed better survival rate. EIF3D stimulated cell proliferation and the number of Edu cells through the activation\u0000 of Warburg effect in vitro model of NHLNHL. Sh-EIF3D diminished NHL cell proliferation and the number of Edu cells through the inactivation of Warburg effect in vitro model of NHL. Then, we found that EIF3D reduced GRP78 protein ubiquitination to induce GRP78/Akt proteins, and\u0000 si-EIF3D promote GRP78 protein ubiquitination to suppress GRP78/Akt proteins in vitro model of NHL. Our results indicate that EIF3D promote NHL cell proliferation throughWarburg effect by the inhibition of GRP78 protein ubiquitination, suggesting that it may prove to be one clinical\u0000 target and pre-tumor gene for NHL.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49119530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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