The purpose of this study was to elucidate the biological role of MicroRNA-223 (miRNA-223) in mediating the malignant progression of esophageal cancer and the underlying mechanism. MiRNA-223 levels were measured using qRT-PCR in 50 paired esophageal cancer tissues and adjacent paracancerous tissues. The correlation between miRNA-223 level and pathological indicators in esophageal cancer patients was analyzed. In vitro experiments assessed the impact of miRNA-223 on the proliferative, migratory, and invasive abilities of esophageal cancer cells. Additionally, rescue experiments were conducted to investigate the involvement of miRNA-223 and its downstream target, SMAD4, in the progression of esophageal cancer. Esophageal cancer tissues showed decreased levels of miRNA-223 compared to adjacent tissues. Patients with low miRNA-223 exhibited higher rates of lymphatic and distant metastasis, as well as poorer overall survival than those with high miRNA-223 levels. Increasing miRNA-223 in TE-1 and EC-109 cells reduced their proliferative, migratory, and invasive capabilities. Esophageal cancer tissues and cell lines displayed elevated SMAD4 levels, which were negatively regulated by miRNA-223. Restoring SMAD4 expression partially reversed the inhibitory effects of miRNA-223 overexpression in esophageal cancer cells. MiRNA-223 is closely correlated to lymphatic metastasis, distant metastasis and poor prognosis of esophageal cancer patients. MiRNA-223 suppresses proliferative, migratory and invasive abilities of esophageal cancer cells via negatively regulating SMAD4.
{"title":"MicroRNA-223 Suppresses the Progression of Esophageal Cancer by Negatively Regulating SMAD Family Member 4","authors":"Jiansheng Lin, Haizhan Shi, Xinyang Zheng, Xiaowei Xie","doi":"10.1166/jbn.2023.3704","DOIUrl":"https://doi.org/10.1166/jbn.2023.3704","url":null,"abstract":"The purpose of this study was to elucidate the biological role of MicroRNA-223 (miRNA-223) in mediating the malignant progression of esophageal cancer and the underlying mechanism. MiRNA-223 levels were measured using qRT-PCR in 50 paired esophageal cancer tissues and adjacent paracancerous tissues. The correlation between miRNA-223 level and pathological indicators in esophageal cancer patients was analyzed. In vitro experiments assessed the impact of miRNA-223 on the proliferative, migratory, and invasive abilities of esophageal cancer cells. Additionally, rescue experiments were conducted to investigate the involvement of miRNA-223 and its downstream target, SMAD4, in the progression of esophageal cancer. Esophageal cancer tissues showed decreased levels of miRNA-223 compared to adjacent tissues. Patients with low miRNA-223 exhibited higher rates of lymphatic and distant metastasis, as well as poorer overall survival than those with high miRNA-223 levels. Increasing miRNA-223 in TE-1 and EC-109 cells reduced their proliferative, migratory, and invasive capabilities. Esophageal cancer tissues and cell lines displayed elevated SMAD4 levels, which were negatively regulated by miRNA-223. Restoring SMAD4 expression partially reversed the inhibitory effects of miRNA-223 overexpression in esophageal cancer cells. MiRNA-223 is closely correlated to lymphatic metastasis, distant metastasis and poor prognosis of esophageal cancer patients. MiRNA-223 suppresses proliferative, migratory and invasive abilities of esophageal cancer cells via negatively regulating SMAD4.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"176 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139301925","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}
Chunyang Xing, Weiping Cai, Yiru Fang, Qikun Wang, Yan Huang, Yuzhe Wang, Weiwei Wang
MiR-16 and other several known oncogenes co-exist in various solid tumors and play carcinogenic roles in many tumors. This study explores whether miR-16 regulates autophagy expression and analyzes the role of targeted nanoparticle intervention in glioma. miR-16 and LC3 expressions were examined by reverse transcription-polymerase chain reaction (RT-PCR). They were assessed in normal lymphocytes, low-metastatic glioma, and high-metastatic glioma cell lines as well. The glioma cell line U251 was used to detect and compare the expression of LC3. Flow cytometry detected cell proliferation and the number of cell invasion and metastasis was detected by Transwell. LC3 mRNA in glioma tissues was evidently increased. The later the Tumor Node Metastasis (TNM) stage, the lower expression of miR-16 and the higher expression of LC3, which is related to TNM stage. LC3 mRNA in glioma cells was obviously higher than normal cells while miR-16 was lower than the latter. The expression of LC3 in glioma cell line U251 was higher, while miR-16 was lower. Transfection of siRNA-LC3 and targeted nanoparticles could effectively down-regulate the level of LC3 in the glioma cell line U251. In conclusion, miR-16 is related to the increased expression of LC3 and the enhanced ability of glioma cells to invade and metastasize.
{"title":"Molecular Mechanism of Inhibition of Glioma by Targeting Autophagy Microtubule-Associated Protein 1A/1B-Light Chain 3 Family via miR-16 with Novel Liposome Nanoparticles","authors":"Chunyang Xing, Weiping Cai, Yiru Fang, Qikun Wang, Yan Huang, Yuzhe Wang, Weiwei Wang","doi":"10.1166/jbn.2023.3712","DOIUrl":"https://doi.org/10.1166/jbn.2023.3712","url":null,"abstract":"MiR-16 and other several known oncogenes co-exist in various solid tumors and play carcinogenic roles in many tumors. This study explores whether miR-16 regulates autophagy expression and analyzes the role of targeted nanoparticle intervention in glioma. miR-16 and LC3 expressions were examined by reverse transcription-polymerase chain reaction (RT-PCR). They were assessed in normal lymphocytes, low-metastatic glioma, and high-metastatic glioma cell lines as well. The glioma cell line U251 was used to detect and compare the expression of LC3. Flow cytometry detected cell proliferation and the number of cell invasion and metastasis was detected by Transwell. LC3 mRNA in glioma tissues was evidently increased. The later the Tumor Node Metastasis (TNM) stage, the lower expression of miR-16 and the higher expression of LC3, which is related to TNM stage. LC3 mRNA in glioma cells was obviously higher than normal cells while miR-16 was lower than the latter. The expression of LC3 in glioma cell line U251 was higher, while miR-16 was lower. Transfection of siRNA-LC3 and targeted nanoparticles could effectively down-regulate the level of LC3 in the glioma cell line U251. In conclusion, miR-16 is related to the increased expression of LC3 and the enhanced ability of glioma cells to invade and metastasize.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"6 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139305437","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}
Jiansheng Hu, Danli Sun, Qinhui Feng, Liang Wei, Wucai Liu
A sandwich electrochemical immunosensor was developed for sensitive detection of carcinoembryonic antigen (CEA) using hollow nanospheres composite material loaded with gold nanoparticles as the signal tag and gold triangular nanoplate as the substrate material. Samples obtained from pediatric solid tumor tissue and their blood samples were used to detect CEA using this nanoparticle. The hollow nanospheres constructed in this study, provided abundant reaction sites and high catalytic activity, while the loading of Au NPs enhances conductivity and biocompatibility. The immunosensor has good analytical ability in detecting CEA in the mass concentration range of 1 pg/mL to 50 ng/mL, with a low detection limit (LOD) of 0.37 pg/mL. This novel method provides a valuable tool for rapid clinical detection of CEA in the context of pediatric solid tumors.
{"title":"Early Detection of Carcinoembryonic Antigen Using Hollow Nanospheres Improves the Outcome of Pediatric Solid Tumors","authors":"Jiansheng Hu, Danli Sun, Qinhui Feng, Liang Wei, Wucai Liu","doi":"10.1166/jbn.2023.3619","DOIUrl":"https://doi.org/10.1166/jbn.2023.3619","url":null,"abstract":"A sandwich electrochemical immunosensor was developed for sensitive detection of carcinoembryonic antigen (CEA) using hollow nanospheres composite material loaded with gold nanoparticles as the signal tag and gold triangular nanoplate as the substrate material. Samples obtained from pediatric solid tumor tissue and their blood samples were used to detect CEA using this nanoparticle. The hollow nanospheres constructed in this study, provided abundant reaction sites and high catalytic activity, while the loading of Au NPs enhances conductivity and biocompatibility. The immunosensor has good analytical ability in detecting CEA in the mass concentration range of 1 pg/mL to 50 ng/mL, with a low detection limit (LOD) of 0.37 pg/mL. This novel method provides a valuable tool for rapid clinical detection of CEA in the context of pediatric solid tumors.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"6 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139294016","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}
Jing Wang, Xin Zhu, Yousef Mirzaei, Fan Zhuo, Hadi Jabbari, Bashar Zuhair Talib Al-Naqeeb, Yao Bai
Melanoma is extremely aggressive and its prevalence is growing every year. Gel was generated by altering thiolated hyaluronic acid on surface-functionalized Pluronic F127-TPGS mixed micelles to create a nanogel with the ability to selectively target melanoma. Cell uptake experiment was used to quantitatively and qualitatively assess the uptake of the nanogel by B16F10 melanoma cells; cytotoxicity experiment was used to investigate the toxicity of the carrier material to cells. Microscopic analysis of the produced nanogel revealed an average particle size of 30 nm, with no discernible cytotoxic effect on both mouse 3T3 fibroblasts and mouse melanoma B16F10 cells. Higher HCAM receptor expression in B16F10 cells allowed for more efficient absorption than in 3T3 cells.
{"title":"Application of Crosslinking of Thiolated Hyaluronic Acid Nanogel for Targeted Therapy and Drug Delivery in Melanoma","authors":"Jing Wang, Xin Zhu, Yousef Mirzaei, Fan Zhuo, Hadi Jabbari, Bashar Zuhair Talib Al-Naqeeb, Yao Bai","doi":"10.1166/jbn.2023.3516","DOIUrl":"https://doi.org/10.1166/jbn.2023.3516","url":null,"abstract":"Melanoma is extremely aggressive and its prevalence is growing every year. Gel was generated by altering thiolated hyaluronic acid on surface-functionalized Pluronic F127-TPGS mixed micelles to create a nanogel with the ability to selectively target melanoma. Cell uptake experiment was used to quantitatively and qualitatively assess the uptake of the nanogel by B16F10 melanoma cells; cytotoxicity experiment was used to investigate the toxicity of the carrier material to cells. Microscopic analysis of the produced nanogel revealed an average particle size of 30 nm, with no discernible cytotoxic effect on both mouse 3T3 fibroblasts and mouse melanoma B16F10 cells. Higher HCAM receptor expression in B16F10 cells allowed for more efficient absorption than in 3T3 cells.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"19 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139296956","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}
In this study, we investigated the impact of FOXN3 on esophageal cancer progression and its underlying mechanism. Through online databases, we observed a significant decrease in FOXN3 levels in esophageal cancer tissues and EC9706 cells. Conversely, SIRT1 expression was elevated in EC109 and EC9706 cells. FOXN3 was found to interact with SIRT1, AKT1, and PIK3CA. To explore FOXN3′s effects, we treated EC9706 cells with pcDNA-FOXN3, which led to increased FOXN3 levels. Consequently, SIRT1, p-AKT/AKT, p-PI3K/PI3K ratios, cell proliferation,migration, invasion, and expression of Ki67, PCNA, MMP3, MMP9, N-cadherin, Vimentin, and Bcl-2 were reduced. In contrast, cell apoptosis, E-cadherin, and Bax levels increased. Further analysis revealed that FOXN3 inhibited cell proliferation and epithelial-mesenchymal transition (EMT) while promoting apoptosis by down-regulating the SIRT1/PI3K/AKT pathway. In conclusion, FOXN3 plays a crucial role in esophageal cancer progression by modulating the SIRT1/PI3K/AKT pathway, affecting cell proliferation, EMT, and apoptosis. This study highlights FOXN3 as a potential target for therapeutic interventions in esophageal cancer.
{"title":"FOXN3: A Novel Tumor Suppressor Inhibits the Progression of Esophageal Cancer via Downregulating the SIRT1/PI3K/AKT Axis","authors":"Liangjun Xue, Chuanxi Wang, Yan Feng","doi":"10.1166/jbn.2023.3694","DOIUrl":"https://doi.org/10.1166/jbn.2023.3694","url":null,"abstract":"In this study, we investigated the impact of FOXN3 on esophageal cancer progression and its underlying mechanism. Through online databases, we observed a significant decrease in FOXN3 levels in esophageal cancer tissues and EC9706 cells. Conversely, SIRT1 expression was elevated in EC109 and EC9706 cells. FOXN3 was found to interact with SIRT1, AKT1, and PIK3CA. To explore FOXN3′s effects, we treated EC9706 cells with pcDNA-FOXN3, which led to increased FOXN3 levels. Consequently, SIRT1, p-AKT/AKT, p-PI3K/PI3K ratios, cell proliferation,migration, invasion, and expression of Ki67, PCNA, MMP3, MMP9, N-cadherin, Vimentin, and Bcl-2 were reduced. In contrast, cell apoptosis, E-cadherin, and Bax levels increased. Further analysis revealed that FOXN3 inhibited cell proliferation and epithelial-mesenchymal transition (EMT) while promoting apoptosis by down-regulating the SIRT1/PI3K/AKT pathway. In conclusion, FOXN3 plays a crucial role in esophageal cancer progression by modulating the SIRT1/PI3K/AKT pathway, affecting cell proliferation, EMT, and apoptosis. This study highlights FOXN3 as a potential target for therapeutic interventions in esophageal cancer.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"32 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139299356","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}
We investigated the role of LINC00312 in pancreatic cancer (PC) and its underlying mechanism. LINC00312 levels were assessed in PC tissues and cell lines using qRT-PCR, and its correlation with clinical indicators was analyzed. Overexpression and knockdown models of LINC00312 were created in PC cell lines. The effects of LINC00312 on PC cell function were evaluated through CCK-8 and Transwell migration assays, and the binding between LINC00312 and the downstream target gene FGD4 was examined using a dual luciferase reporter gene assay. LINC00312 levels were significantly lower in PC tissues compared to adjacent tissues. High LINC00312 levels were associated with increased incidence of lymphatic and distant metastasis. PC cell lines exhibited downregulated LINC00312 expression. LINC00312 overexpression reduced cell proliferation and migration, while knockdown had the opposite effect. Bioinformatics analysis and luciferase reporter assays confirmed that LINC00312 binds to FGD4. Western blot analysis revealed reduced FGD4 levels upon LINC00312 overexpression, and a negative correlation between FGD4 and LINC00312 expression in PC. Moreover, FGD4 promoted PC cell proliferation and migration, its overexpression counteracted the inhibitory effects of LINC00312 overexpression on PC progression. Downregulation of LINC00312 in PC tissues and cell lines. LINC00312 overexpression suppresses PC cell proliferation and migration by negatively regulating FGD4. Thus, LINC00312 represents a potential therapeutic target for PC.
我们研究了LINC00312在胰腺癌（PC）中的作用及其内在机制。我们使用 qRT-PCR 技术评估了 PC 组织和细胞系中的 LINC00312 水平，并分析了其与临床指标的相关性。在PC细胞系中创建了LINC00312的过表达和敲除模型。通过CCK-8和Transwell迁移试验评估了LINC00312对PC细胞功能的影响，并使用双荧光素酶报告基因试验检测了LINC00312与下游靶基因FGD4之间的结合。与邻近组织相比，PC组织中的LINC00312水平明显较低。高水平的LINC00312与淋巴转移和远处转移的发生率增加有关。PC细胞系的LINC00312表达下调。LINC00312过表达会降低细胞的增殖和迁移，而敲除则会产生相反的效果。生物信息学分析和荧光素酶报告实验证实，LINC00312与FGD4结合。Western印迹分析表明，LINC00312过表达时FGD4水平降低，PC中FGD4和LINC00312的表达呈负相关。此外，FGD4能促进PC细胞的增殖和迁移，其过表达能抵消LINC00312过表达对PC进展的抑制作用。PC 组织和细胞系中 LINC00312 的下调。LINC00312过表达可通过负调控FGD4抑制PC细胞的增殖和迁移。因此，LINC00312 是治疗 PC 的潜在靶点。
{"title":"Long Intergenic Non-Protein Coding RNA 312 Regulates FRABIN to Inhibit the Occurrence and Development of Pancreatic Cancer","authors":"Jigang Bai, Xin Wang, Xiaoqiang Dai","doi":"10.1166/jbn.2023.3699","DOIUrl":"https://doi.org/10.1166/jbn.2023.3699","url":null,"abstract":"We investigated the role of LINC00312 in pancreatic cancer (PC) and its underlying mechanism. LINC00312 levels were assessed in PC tissues and cell lines using qRT-PCR, and its correlation with clinical indicators was analyzed. Overexpression and knockdown models of LINC00312 were created in PC cell lines. The effects of LINC00312 on PC cell function were evaluated through CCK-8 and Transwell migration assays, and the binding between LINC00312 and the downstream target gene FGD4 was examined using a dual luciferase reporter gene assay. LINC00312 levels were significantly lower in PC tissues compared to adjacent tissues. High LINC00312 levels were associated with increased incidence of lymphatic and distant metastasis. PC cell lines exhibited downregulated LINC00312 expression. LINC00312 overexpression reduced cell proliferation and migration, while knockdown had the opposite effect. Bioinformatics analysis and luciferase reporter assays confirmed that LINC00312 binds to FGD4. Western blot analysis revealed reduced FGD4 levels upon LINC00312 overexpression, and a negative correlation between FGD4 and LINC00312 expression in PC. Moreover, FGD4 promoted PC cell proliferation and migration, its overexpression counteracted the inhibitory effects of LINC00312 overexpression on PC progression. Downregulation of LINC00312 in PC tissues and cell lines. LINC00312 overexpression suppresses PC cell proliferation and migration by negatively regulating FGD4. Thus, LINC00312 represents a potential therapeutic target for PC.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"8 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139297137","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}
Jie Zhang, Zhihui Sheng, Hao Zhang, Wenwen Qi, Tao Jia
In this study, we investigated the role of miR-301b-3p in promoting tumor cell proliferation and metastasis and explored the anti-cancer effects of quercetin in laryngocarcinoma cells. Through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation analyses, we examined the effects of miR-301b-3p and PTEN on potential target genes. We measured laryngocarcinoma cell activity and apoptosis using CCK8 and flow cytometry, respectively, and assessed migration and invasion through transwell assay. qRT-PCR was used to determine the levels of miR-301b-3p and PTEN in laryngocarcinoma cells. Luciferase activity and western blot assays were employed to study the interaction between miR-301b-3p and PTEN. We found that miR-301b-3p was associated with various types of cancer, and pathways related to miR-301b-3p overlapped with those of PTEN. Quercetin effectively inhibited the proliferation, migration, and invasion of laryngocarcinoma cells, but these effects were reversed by miR-301b-3p overexpression. The level of miR-301b-3p was significantly increased in laryngocarcinoma cells, leading to down-regulation of PTEN protein and enhanced tumor cell activity. However, restoring PTEN alleviated the malignant growth caused by miR-301b-3p overexpression. Ultimately, quercetin exerted its inhibitory effects on proliferation, migration, and invasion by regulating the miR-301b-3p/PTEN axis in laryngocarcinoma cells. These findings highlight the potential of quercetin as a promising treatment option for laryngocarcinoma.
{"title":"Quercetin Inhibits Proliferation and Migration via miR-301b-3p/Phosphatase and Tensin Homolog Axis Regulation in Laryngocarcinoma Cells","authors":"Jie Zhang, Zhihui Sheng, Hao Zhang, Wenwen Qi, Tao Jia","doi":"10.1166/jbn.2023.3703","DOIUrl":"https://doi.org/10.1166/jbn.2023.3703","url":null,"abstract":"In this study, we investigated the role of miR-301b-3p in promoting tumor cell proliferation and metastasis and explored the anti-cancer effects of quercetin in laryngocarcinoma cells. Through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation analyses, we examined the effects of miR-301b-3p and PTEN on potential target genes. We measured laryngocarcinoma cell activity and apoptosis using CCK8 and flow cytometry, respectively, and assessed migration and invasion through transwell assay. qRT-PCR was used to determine the levels of miR-301b-3p and PTEN in laryngocarcinoma cells. Luciferase activity and western blot assays were employed to study the interaction between miR-301b-3p and PTEN. We found that miR-301b-3p was associated with various types of cancer, and pathways related to miR-301b-3p overlapped with those of PTEN. Quercetin effectively inhibited the proliferation, migration, and invasion of laryngocarcinoma cells, but these effects were reversed by miR-301b-3p overexpression. The level of miR-301b-3p was significantly increased in laryngocarcinoma cells, leading to down-regulation of PTEN protein and enhanced tumor cell activity. However, restoring PTEN alleviated the malignant growth caused by miR-301b-3p overexpression. Ultimately, quercetin exerted its inhibitory effects on proliferation, migration, and invasion by regulating the miR-301b-3p/PTEN axis in laryngocarcinoma cells. These findings highlight the potential of quercetin as a promising treatment option for laryngocarcinoma.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"46 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139297876","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}
Yiyu Hong, Zhaozhong Xu, Yantao Zheng, Jing Liu, Zhenhui Huang, Jiasong Chen, Yao Zhang, Bin Liu
The aim of this study was to investigate the protective effect of Ferristatin II (Fer II) on ferric ammonium citrate (FAC)-induced ferroptosis and explore its mechanism by performing experiments in vitro. The cell viability of Fer II in the treatment of FAC-induced ferroptosis was investigated by MTT, measuring the concentrations of Fe2+ and MDA and the activity of CSH-PX. We further measured the protein expression of hepcidin (Hepc), TfR1, BMP6, p-Smad1 and p-Smad5 using Western blotting. The gene expression level of Hepc was significantly increased and the protein expression levels of p-SMAD1 and p-SMAD5 were also significantly up-regulated after the coordinated intervention of Fer II and BMP. The results showed that cell viability was increased after treatment with Fer II. The concentrations of Fe2+ and MDA revealed that Fer II decreased hepatocyte ferroptosis induced by FAC. The Western blot results also showed that Fer II up-regulated the protein expression of Hepc and down-regulated protein expression of TfR1, BMP6, p-Smad1 and p-Smad5. Further results showed that Fer II and BMP6 synergistically promoted Hepc secretion and up-regulated the protein expression levels of Smad1 and p-Smad5. Fer II alleviated FAC-induced ferroptosis in HepG2 cells by regulating the BMP6/SMAD pathway, suggesting a new therapeutic approach for hepatocyte protection.
本研究旨在通过体外实验研究铁锈素Ⅱ（FerⅡ）对柠檬酸铁铵（FAC）诱导的铁中毒的保护作用及其机制。我们用 MTT 检测了 Fer II 在治疗 FAC 诱导的铁中毒中的细胞活力，测量了 Fe2+ 和 MDA 的浓度以及 CSH-PX 的活性。我们还用 Western 印迹法测定了肝素（Hepc）、TfR1、BMP6、p-Smad1 和 p-Smad5 的蛋白表达。在 Fer II 和 BMP 的协同干预下，Hepc 的基因表达水平明显提高，p-SMAD1 和 p-SMAD5 的蛋白表达水平也明显上调。结果表明，Fer II 处理后细胞活力增加。Fe2+和MDA的浓度显示，Fer II降低了FAC诱导的肝细胞铁变态反应。Western 印迹结果还显示，Fer II 上调了 Hepc 的蛋白表达，下调了 TfR1、BMP6、p-Smad1 和 p-Smad5 的蛋白表达。进一步的结果表明，Fer II 和 BMP6 协同促进了 Hepc 的分泌，并上调了 Smad1 和 p-Smad5 的蛋白表达水平。Fer II通过调节BMP6/SMAD通路缓解了FAC诱导的HepG2细胞铁变态反应，为保护肝细胞提供了一种新的治疗方法。
{"title":"Ferristatin II Inhibits Ferroptosis by Regulating the Bone Morphogenetic Protein 6/SMAD Signaling Pathway in HepG2 Cells","authors":"Yiyu Hong, Zhaozhong Xu, Yantao Zheng, Jing Liu, Zhenhui Huang, Jiasong Chen, Yao Zhang, Bin Liu","doi":"10.1166/jbn.2023.3705","DOIUrl":"https://doi.org/10.1166/jbn.2023.3705","url":null,"abstract":"The aim of this study was to investigate the protective effect of Ferristatin II (Fer II) on ferric ammonium citrate (FAC)-induced ferroptosis and explore its mechanism by performing experiments in vitro. The cell viability of Fer II in the treatment of FAC-induced ferroptosis was investigated by MTT, measuring the concentrations of Fe2+ and MDA and the activity of CSH-PX. We further measured the protein expression of hepcidin (Hepc), TfR1, BMP6, p-Smad1 and p-Smad5 using Western blotting. The gene expression level of Hepc was significantly increased and the protein expression levels of p-SMAD1 and p-SMAD5 were also significantly up-regulated after the coordinated intervention of Fer II and BMP. The results showed that cell viability was increased after treatment with Fer II. The concentrations of Fe2+ and MDA revealed that Fer II decreased hepatocyte ferroptosis induced by FAC. The Western blot results also showed that Fer II up-regulated the protein expression of Hepc and down-regulated protein expression of TfR1, BMP6, p-Smad1 and p-Smad5. Further results showed that Fer II and BMP6 synergistically promoted Hepc secretion and up-regulated the protein expression levels of Smad1 and p-Smad5. Fer II alleviated FAC-induced ferroptosis in HepG2 cells by regulating the BMP6/SMAD pathway, suggesting a new therapeutic approach for hepatocyte protection.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"48 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139302887","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}
Role of ferroptosis in acute kidney injury (AKI) is not fully uncovered. We aim to explore a novel role that SNHG11/miR-324-3p modulated ferroptosis in AKI via modulating GPX4. To mimic AKI in vivo, 6-week male C57BL/6 mice were administrated with lipopolysaccharide (LPS). shRNA (sh-NC or sh-SNHG11), miRNA antagomir (antagomir-NC or miR-324-3p antagomir), miRNA agomir (agomir-NC and miR-324-3p agomir) were injected in mice to regulate SNHG11 and miR-324-3p, respectively. To stimulate the in vitro model of AKI, HK-2 cells were incubated with LPS for 6 h, followed by the transfection with shRNA (sh-NC or sh-SNHG11), miRNA mimics (mimics-NC or miR-324-3p mimics), miRNA inhibitor (inhibitor-NC and miR-324-3p inhibitor), respectively. Co-transfection of miR-324-3p mimics and SNHG11-wt decreased the relative luciferase activity, suggesting miR-324-3p was the target of SNHG11. SNHG11 silence increased miR-324-3p expression in LPS-stimulated HK-2 cells. Both of SNHG11 silence and miR-324-3p upregulation aggravated LPS-induced ferroptosis and kidney injury, and decreased GPX4 whereas downregulation of miR-324-3p inhibited LPS-caused impairment, and increased GPX4 in AKI models. In AKI models with SNHG11 silence, upregulation of miR-324-3p further enhanced ferroptosis and kidney injury, and resulted in the lower expression of GPX4. Decreased SNHG11 caused miR-324-3p upregulation in renal tubular epithelial cells, which led to GPX4 reduction that trigger ferroptosis in AKI.
{"title":"LncRNA Small Nucleolar RNA Host Gene 11 Modulates Ferroptosis in Renal Tubular Epithelial Cells via miR-324-3p/GPX4 Axis in Acute Kidney Injury","authors":"Xin Li, Lei Zhang, Guixiang Chen","doi":"10.1166/jbn.2023.3701","DOIUrl":"https://doi.org/10.1166/jbn.2023.3701","url":null,"abstract":"Role of ferroptosis in acute kidney injury (AKI) is not fully uncovered. We aim to explore a novel role that SNHG11/miR-324-3p modulated ferroptosis in AKI via modulating GPX4. To mimic AKI in vivo, 6-week male C57BL/6 mice were administrated with lipopolysaccharide (LPS). shRNA (sh-NC or sh-SNHG11), miRNA antagomir (antagomir-NC or miR-324-3p antagomir), miRNA agomir (agomir-NC and miR-324-3p agomir) were injected in mice to regulate SNHG11 and miR-324-3p, respectively. To stimulate the in vitro model of AKI, HK-2 cells were incubated with LPS for 6 h, followed by the transfection with shRNA (sh-NC or sh-SNHG11), miRNA mimics (mimics-NC or miR-324-3p mimics), miRNA inhibitor (inhibitor-NC and miR-324-3p inhibitor), respectively. Co-transfection of miR-324-3p mimics and SNHG11-wt decreased the relative luciferase activity, suggesting miR-324-3p was the target of SNHG11. SNHG11 silence increased miR-324-3p expression in LPS-stimulated HK-2 cells. Both of SNHG11 silence and miR-324-3p upregulation aggravated LPS-induced ferroptosis and kidney injury, and decreased GPX4 whereas downregulation of miR-324-3p inhibited LPS-caused impairment, and increased GPX4 in AKI models. In AKI models with SNHG11 silence, upregulation of miR-324-3p further enhanced ferroptosis and kidney injury, and resulted in the lower expression of GPX4. Decreased SNHG11 caused miR-324-3p upregulation in renal tubular epithelial cells, which led to GPX4 reduction that trigger ferroptosis in AKI.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"32 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139297487","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}
Jian Wang, Bo Zheng, Shu Yang, Fuqiang Guo, Binghu Li, Duo-zi Wang, Jianhong Wang
This study mainly explored the amelioratory effect of silica-coated superparamagnetic iron oxide nanoparticles (SiO4@SPIONs) on leukoaraiosis-associated cognitive dysfunction via targeting of Nrf2 and their potential mechanism. PC12 cell line was given in vitro hypoxia-reoxygenation treatment (OGD/R) and divided into normal group, model group and SiO4@SPIONs treatment group. The cell survival rate, apoptosis rate, levels of ROS (reactive oxygen species), MDA (Malondialdehyde; malonic dialdehyde; Propanedial) and anti-oxidases were monitored. Western-blotting measured the level of Akt and Nrf2. The Akt-targeting antagonist LY294002 was applied for verifying the regulatory effect of SiO4@SPIONs. In comparison with normal cells, model cells exhibited significantly reduced viability, along with significantly elevated apoptosis rate. Meanwhile, model cells also displayed elevated levels of intracellular ROS and MDA, with diminished levels of SOD (Superoxide Dismutase), GSH (glutathione), CAT (Computerized Axial Tomography) and GSH-Px (glutathione peroxidase) which were accompanied by significantly weakened phosphorylation level of Akt. Lastly, model cells also exhibited moderate enhancement of Nrf2 and HO-1 expressions. Moreover, cells in SiO4@SPIONs treatment group exhibited significantly increased viability, along with reduced apoptosis rate. Meanwhile, the cells in the SiO4@SPIONs treatment group also displayed decreased levels of intracellular ROS and MDA, while showing increased levels of SOD, GSH, CAT and GSH-Px, which were accompanied by significantly increased Akt phosphorylation and Nrf2 and HO-1 expressions. The SiO4@SPIONS can ameliorate the leukoaraiosis-triggered oxidative stress via targeting of Nrf2 to activate the IRS-1/Akt signals.
{"title":"Silica-Coated Superparamagnetic Iron Oxide Nanoparticles Ameliorate Leukoaraiosis-Triggered Oxidative Stress via Targeting of Nrf2 to Activate IRS-1/Akt Signals","authors":"Jian Wang, Bo Zheng, Shu Yang, Fuqiang Guo, Binghu Li, Duo-zi Wang, Jianhong Wang","doi":"10.1166/jbn.2023.3708","DOIUrl":"https://doi.org/10.1166/jbn.2023.3708","url":null,"abstract":"This study mainly explored the amelioratory effect of silica-coated superparamagnetic iron oxide nanoparticles (SiO4@SPIONs) on leukoaraiosis-associated cognitive dysfunction via targeting of Nrf2 and their potential mechanism. PC12 cell line was given in vitro hypoxia-reoxygenation treatment (OGD/R) and divided into normal group, model group and SiO4@SPIONs treatment group. The cell survival rate, apoptosis rate, levels of ROS (reactive oxygen species), MDA (Malondialdehyde; malonic dialdehyde; Propanedial) and anti-oxidases were monitored. Western-blotting measured the level of Akt and Nrf2. The Akt-targeting antagonist LY294002 was applied for verifying the regulatory effect of SiO4@SPIONs. In comparison with normal cells, model cells exhibited significantly reduced viability, along with significantly elevated apoptosis rate. Meanwhile, model cells also displayed elevated levels of intracellular ROS and MDA, with diminished levels of SOD (Superoxide Dismutase), GSH (glutathione), CAT (Computerized Axial Tomography) and GSH-Px (glutathione peroxidase) which were accompanied by significantly weakened phosphorylation level of Akt. Lastly, model cells also exhibited moderate enhancement of Nrf2 and HO-1 expressions. Moreover, cells in SiO4@SPIONs treatment group exhibited significantly increased viability, along with reduced apoptosis rate. Meanwhile, the cells in the SiO4@SPIONs treatment group also displayed decreased levels of intracellular ROS and MDA, while showing increased levels of SOD, GSH, CAT and GSH-Px, which were accompanied by significantly increased Akt phosphorylation and Nrf2 and HO-1 expressions. The SiO4@SPIONS can ameliorate the leukoaraiosis-triggered oxidative stress via targeting of Nrf2 to activate the IRS-1/Akt signals.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"18 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139299449","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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