{"title":"Evaluation of t-DARPP Expression Alteration in Association with DDR1 Expression in Non-Small Cell Lung Cancer.","authors":"Zahra Damavandi, Pardis Riahi, Tayebeh Majidizadeh, Massoud Houshmand","doi":"10.61186/ibj.3878","DOIUrl":"10.61186/ibj.3878","url":null,"abstract":"<p><strong>Background: </strong>Discoidin domain receptor 1 (DDR1) signaling plays a critical role in various cellular functions. Increased DDR1 expression has been shown in different human cancers. t-DARPP is a truncated isoform of DARPP-32, and its upregulation promotes cell survival and migration. Most lung cancer patients have non-small cell lung cancer (NSCLC), and their survival rate is low. Therefore, it is necessary to study new and effective targeted therapies. Increased t-DARPP expression in NSCLC patients is associated with patient survival and can act as a prognostic marker correlated with increasing stages of NSCLC. The current study aimed to evaluate alteration in DDR1 expression and its effects on t-DARPP expression in NSCLC.</p><p><strong>Methods: </strong>Two human lung adenocarcinoma cell lines, A549 and Calu-3, were treated with collagen type I and transfected with DDR1 siRNA. The relative expression of DDR1 and t-DARPP was evaluated using qRT-PCR.</p><p><strong>Results: </strong>The results indicated that collagen type I could stimulate DDR1 expression in NSCLC cells. Also, DDR1 upregulation resulted in a significant increase in t-DARPP expression. In contrast, suppression of DDR1 expression significantly decreased t-DARPP expression.</p><p><strong>Conclusion: </strong>Our findings propose that modification in the expression of DDR1, caused by collagen type I and siRNA, might influence the expression of t-DARPP in NSCLC that is linked to NSCLC progression. Moreover, this alteration could potentially serve as an innovative target for therapeutic intervention.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10994641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139671759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Melittin as an Activator of the Autophagy and Unfolded Protein Response Pathways in Colorectal HCT116 Cell Line.","authors":"Mozhdeh Zamani, Farzaneh Bozorg-Ghalati, Pooneh Mokarram","doi":"10.61186/ibj.3993","DOIUrl":"10.61186/ibj.3993","url":null,"abstract":"<p><strong>Background: </strong>The potential anticancer effect of melittin has motivated scientists to find its exact molecular mechanism of action. There are few data on the effect of melittin on the UPR and autophagy as two critical pathways involved in tumorigenesis of colorectal and drug resistance. This study aimed to investigate the effect of melittin on these pathways in the colorectal cancer (CRC) HCT116 cells.</p><p><strong>Methods: </strong>MTT method was carried out to assess the cytotoxicity of melittin on the HCT116 cell line for 24, 48, and 72 h. After selecting the optimal concentrations and treatment times, the gene expression of autophagy flux markers (LC3-βII and P62) and UPR markers (CHOP and XBP-1s) were determined using qRT-PCR. The protein level of autophagy initiation marker (Beclin1) was also determined by Western blotting.</p><p><strong>Results: </strong>MTT assay showed a cytotoxic effect of melittin on the HCT116 cells. The increase in LC3-βII and decrease in P62 mRNA expression levels, along with the elevation in the Beclin1 protein level, indicated the stimulatory role of melittin on the autophagy. Melittin also significantly enhanced the CHOP and XBP-1s expressions at mRNA level, suggesting the positive role of the melittin on the UPR activation.</p><p><strong>Conclusion: </strong>This study shows that UPR and autophagy can potentially be considered as two key signaling pathways in tumorigenesis, which can be targeted by the BV melittin in the HCT116 cells. Further in vivo evaluations are recommended to verify the obtained results.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10994640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140039324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Celiac Disease: A Review from Genetic to Treatment.","authors":"Erfaneh Jafari, Niloufar Soleymani, Masoud Hamidi, Azar Rahi, Akram Rezaei, Reza Azizian","doi":"10.61186/ibj.4028","DOIUrl":"10.61186/ibj.4028","url":null,"abstract":"<p><p>Celiac disease (CD) is a complex disorder influenced by genetic and environmental factors. When people with a genetic predisposition to CD consume gluten, an inflammatory response is triggered in the small intestine, and this reaction can be alleviated by the elimination of gluten from the diet. The clinical manifestations of CD vary greatly from person to person and begin at a young age or in adulthood. Influence of genetic factors on CD development is evident in carriers of the DQ2 and/or DQ8 allele. HLA genotypes are associated with gut colonization by bacteria, particularly in individuals suffering from CD. In addition, beneficial gut microbes are crucial for the production of DPP-4, which plays a key role in immune function, as well as metabolic and intestinal health. Therefore, probiotics have been recommended as a complementary food supplement in CD.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10994635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140039323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Methylation Status of miR-34a and miR-126 in Non-Small Cell Lung Cancer (NSCLC) Tumor Tissues.","authors":"Nazanin Mehrzad, Mohammad Saber Zamani, Amirabbas Rahimi, Masoud Shamaei, Morteza Karimipoor","doi":"10.61186/ibj.3845","DOIUrl":"10.61186/ibj.3845","url":null,"abstract":"<p><strong>Background: </strong>MiR-34a and miR-126 mainly act as tumor suppressors and are often downregulated in various cancers, including non-small cell lung cancer (NSCLC). We aimed to determine the methylation status of miR-34a and miR-126 in NSCLC patients.</p><p><strong>Methods: </strong>The current study included 63 paraffin-embedded NSCLC and paired adjacent normal tissues. After DNA extraction and bisulfite treatment, the methylation status of miR-34a and miR-126 were evaluated using the MSP method.</p><p><strong>Results: </strong>There was no statistically significant difference between tumor and normal tissues regarding the methylation status of miR-34a and miR-126 (p > 0.05). Moreover, we found no significant correlation between the methylation status of miR-34a and miR-126 with patients’ demographic parameters, including gender, age, and pathology subtype (p > 0.05).</p><p><strong>Conclusion: </strong>Considering the low expression of mir-126 and mir-34 in NSCLC, more sensitive methods are recommended to be exploited for detecting the level of methylation or underlying mechanisms other than promoter hypermethylation in silencing these genes in NSCLC.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10994634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140039325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Evaluation of Anti-Bacterial and Anti-Biofilm Activity of Native Probiotic Strains of Lactobacillus Extracts.","authors":"Elmira Karimzadeh Barenji, Shokufeh Beglari, Azar Tahghighi, Parisa Azerang, Mahdi Rohani","doi":"10.61186/ibj.4043","DOIUrl":"10.61186/ibj.4043","url":null,"abstract":"<p><strong>Background: </strong>Lactic acid bacteria produce various beneficial metabolites, including antimicrobial agents. Owing to the fast-rising antibiotic resistance among pathogenic microbes, scientists are exploring antimicrobials beyond antibiotics. In this study, we examined four Lactobacillus strains, namely L. plantarum 42, L. brevis 205, L. rhamnosus 239, and L. delbrueckii 263, isolated from healthy human microbiota, to evaluate their antibacterial and antifungal activity.</p><p><strong>Methods: </strong>Lactobacillus strains were cultivated, and the conditioned media were obtained. The supernatant was then used to treat pathogenic bacteria and applied to the growth media containing fungal and bacterial strains. Additionally, the supernatant was separated to achieve the organic and aqueous phases. The two phases were then examined in terms of bacterial and fungal growth rates. Disk diffusion and MIC tests were conducted to determine strains with the most growth inhibition potential. Finally, the potent strains identified through the MIC test were tested on the pathogenic microorganisms to assess their effects on the formation of pathogenic biofilms.</p><p><strong>Results: </strong>The organic phase of L. rhamnosus 239 extracts exhibited the highest antibacterial and antibiofilm effects, while that of L. brevis 205 demonstrated the most effective antifungal impact, with a MIC of 125 µg/mL against Saccharomyces cerevisiae.</p><p><strong>Conclusion: </strong>This study confirms the significant antimicrobial impacts of the lactic acid bacteria strains on pathogenic bacteria and fungi; hence, they could serve as a reliable alternative to antibiotics for a safe and natural protection against pathogenic microorganisms.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11186614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141288052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mutations in COL6A Gene Family Responsible for Muscular Dystrophies in Three Unrelated Families.","authors":"Nasibeh Soltani, Zahra Shahbazi, Morteza Karimipoor, Mohammad Sadegh Fallah, Fatemeh Zafarghandi Motlagh, Masoume Amini, Mojdeh Jamali, Hamideh Bagherian, Razie Zeinali, Sirous Zeinali","doi":"10.61186/ibj.4018","DOIUrl":"https://doi.org/10.61186/ibj.4018","url":null,"abstract":"<p><strong>Background: </strong>Muscular dystrophy is an inherited disease with clinical and genetic heterogeneity. Muscle weakness is the primary symptom of these disorders that often leads to disability and death. The overall prevalence for all types of muscular dystrophies worldwide is 19.8-25.1 per 100,000 population. Autosomal recessive types of muscular dystrophies are more common in Iran, likely due to the high rate of consanguineous marriage. We aimed at deciphering molecular defects in three unrelated families with muscular dystrophies not related to Duchene MD or limb girdle muscular dystrophies. We are reporting families having affected children with MD owing to the mutations in three genes related to the COL6A (collagen type VI, alpha subunit) gene family.</p><p><strong>Methods: </strong>Three unrelated families, who had at least one member affected with MD and for whom a definite molecular diagnosis was not provided by routine methods, were investigated by WES and confirmed by Sanger sequencing.</p><p><strong>Results: </strong>In the first family, a homozygous variant was found in the COL6A3 gene (NM_004369.4:c.4390C>T:p.Arg1464Ter), which explains the clinical symptoms observed in this family. In the second family, two homozygote missense variants with possible relevance to the patient’s phenotype were identified in COL6A1 and COL6A2 genes (NM_001848.2:c.803A>G: p.Glu268Gly and NM_001849.3:c.2489G>A:p.Arg830Gln). Also, a heterozygous pathogenic variant in the COL6A2 gene (NM_001849.3: c.1053+1G>T) was detected in the third family.</p><p><strong>Conclusion: </strong>WES can serve as an effective method for detecting the causative mutations in families with unresolved cases of MD. The data provided herein broadens the spectrum of mutations causing MD in Iran.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142465524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Evaluation of Vascular Endothelial Growth Factor Gene Expression in Recellularized Liver Tissue by Mouse Embryo Fibroblast.","authors":"Motahare Homayoon Vala, Hamed Bagheri, Sargazi Zinat, Negar Bakhtiary, Shahram Pourbeiranvand, Mojdeh Salehnia","doi":"10.61186/ibj.3862","DOIUrl":"10.61186/ibj.3862","url":null,"abstract":"<p><strong>Background: </strong>The aim of the present study was to evaluate alterations in the vegf gene expression as an angiogenic factor in mouse embryo fibroblasts seeded on the decellularized liver fragments.</p><p><strong>Methods: </strong>Liver tissue samples (n = 10) collected from adult male mice were randomly divided into decellularized and native control groups. Tissues were decellularized by treating with 1% Triton X-100 and 0.1% SDS for 24 hours and assessed by H&E staining and SEM. Then DNA content analysis and toxicity tests were performed. By centrifugation, DiI-labeled mouse embryo fibroblasts were seeded on each scaffold and cultured for one week. The recellularized scaffolds were studied by H&E staining, SEM, and LSCM. After RNA extraction and cDNA synthesis, the expression of the vegf gene in these samples was investigated using real-time RT-PCR.</p><p><strong>Results: </strong>Our observations showed that the decellularized tissues had morphology and porous structure similar to the control group, and their DNA content significantly reduced (p < 0.05) and reached to 4.12% of the control group. The MTT test indicated no significant cellular toxicity for the decellularized scaffolds. Light microscopy, SEM, and LSCM observations confirmed the attachment and penetration of embryonic fibroblast cells on the surface and into different depths of the scaffolds. There was no statistically significant difference in terms of vegf gene expression in the cultured cells in the presence and absence of a scaffold.</p><p><strong>Conclusion: </strong>The reconstructed scaffold had no effect on vegf gene expression. Decellularized mouse liver tissue recellularized by embryonic fibroblasts could have an application in regenerative medicine.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10826915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72209309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Nona-Arginine Mediated Anti-E6 ShRNA Delivery Suppresses the Growth of Hela Cells in vitro.","authors":"Razieh Taghizadeh Pirposhteh, Ehsan Arefian, Arash Arashkia, Nasir Mohajel","doi":"10.61186/ibj.3963","DOIUrl":"10.61186/ibj.3963","url":null,"abstract":"<p><strong>Background: </strong>The E6 oncoprotein of HPV plays a crucial role in promoting cell proliferation and inhibiting apoptosis, leading to tumor growth. Non-viral vectors such as nona-arginine (R9) peptides have shown to be potential as carriers for therapeutic molecules. This study aimed to investigate the efficacy of nona-arginine in delivering E6 shRNA and suppressing the E6 gene of HeLa cells in vitro.</p><p><strong>Methods: </strong>HeLa cells carrying E6 gene were treated with a complex of nona-arginine and E6 shRNA. The complex was evaluated using gel retardation assay and FESEM microscopy. The optimal N/P ratio for R9 peptide to transfect HeLa cells with luciferase gene was determined. Relative real-time PCR was used to evaluate the efficiency of mRNA suppression efficiency for E6 shRNA, while the effect of E6 shRNA on cell viability was measured using an MTT assay.</p><p><strong>Results: </strong>The results indicated that R9 efficiently binds to shRNA and effectively transfects E6 shRNA complexes at N/P ratios greater than 30. Transfection with R9 and PEI complexes resulted in a significant toxicity compared to the scrambled plasmid, indicating selective toxicity for HeLa cells. Real-time PCR confirmed the reduction of E6 mRNA expression levels in the cells transfected with anti-E6 shRNA.</p><p><strong>Conclusion: </strong>The study suggests that R9 is a promising non-viral gene carrier for transfecting E6 shRNA in vitro, with significant transfection efficiency and minimal toxicity.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10826911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136397350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Increased Expression of NOTCH-1 and T Helper Cell Transcription Factors in Patients with Acquired Aplastic Anemia.","authors":"Vandana Sharma, Manju Namdeo, Prabin Kumar, Dipendra Kumar Mitra, Parthaprasad Chattopadhyay, Sudha Sazawal, Rekha Chaubey, Renu Saxena, Uma Kanga, Tulika Seth","doi":"10.61186/ibj.3754","DOIUrl":"10.61186/ibj.3754","url":null,"abstract":"<p><strong>Background: </strong>Acquired aplastic anemia is an autoimmune disease in which auto-aggressive T cells destroy hematopoietic progenitors. T-cell differentiation is controlled by transcription factors that interact with NOTCH-1, which influences the respective T-cell lineages. Notch signaling also regulates the BM microenvironment. The present study aimed to assess the gene expressions of NOTCH-1 and T helper cell transcription factors in the acquired aplastic anemia patients.</p><p><strong>Methods: </strong>Using quantitative real-time PCR, we studied the mRNA expression level for NOTCH-1, its ligands (DLL-1 and JAG-1), and T helper cell transcription factors (T-BET, GATA-3, and ROR-γt) in both PB and BM of aAA patients and healthy controls. Further, patients of aplastic anemia were stratified by their disease severity as per the standard criteria.</p><p><strong>Results: </strong>The mRNA expression level of NOTCH-1, T-BET, GATA-3, and ROR-γT genes increased in aAA patients compared to healthy controls. There was no significant difference in the mRNA expression of Notch ligands between patients and controls. The mRNA expression level of the above-mentioned genes was found to be higher in SAA and VSAA than NSAA patients. In addition, NOTCH-1 and T helper cell-specific transcription factors enhanced in aAA. We also observed a significant correlation between the genes and hematological parameters in patients.</p><p><strong>Conclusion: </strong>The interaction between NOTCH-1, T-BET, GATA-3, and ROR-γT might lead to the activation, proliferation, and polarization of T helper cells and subsequent BM destruction. The mRNA expression levels of genes varied with disease severity, which may contribute to pathogenesis of aAA.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10826914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138046908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Role of High-Fructose Diet in Liver Function of Rodent Models: A Systematic Review of Molecular Analysis.","authors":"Roya Mirzaei, Roya Khosrokhavar, Sepideh Arbabi Bidgoli","doi":"10.52547/ibj.3965","DOIUrl":"10.52547/ibj.3965","url":null,"abstract":"<p><p>The present systematic review of animal studies on long-term fructose intake in rodents revealed a significant decrease in the activities of antioxidant enzymes due to a fructose-rich diet. The reduced activity of these enzymes led to an increase in oxidative stress, which can cause liver damage in rodents. Of eight studies analyzed, 5 (62.5%) and 1 (12.5%) used male and female rats, respectively, while 2 studies (25%) used female mice. Moreover, half of the studies used HFCS, but the other half employed fructose in the diet. Hence, it is essential to monitor dietary habits to ensure public health and nutrition research outcomes.</p>","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10826909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139402831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}