Background: Breast cancer is the most frequent malignancy in women worldwide and occurs when cells in the breast begin to grow out of control. Matrix metalloproteinases (MMP), including MMP1 protein, are important in the progression of various types of cancer. Quinacrine, a derivative of 9-aminoacridine, has been shown to inhibit the growth of several types of cancer cells. In this study, we examined the effect of Quinacrine on MMP1 gene expression in breast cancer cell lines MDA-MB 231 and MCF7. MDA-MB 231 cell line has triple negative breast cancer cells properties. Materials and Methods: Breast cancer cell lines, MDA-MB 231 and MCF7, were treated with 0. 5 μ M Quinacrine for 3 days. The dose was selected using MTT assay. Expression of MMP1 gene was quantified by Real-time PCR. Significance of observations were statistically checked by t-test using P<0. 05 as the level of significance. Results: Quinacrine did not have meaningful effect on MMP1 gene expression on MDAMB 231 and MCF7 cell lines in 0. 5 μ M concentration for 72 hours. Conclusion: MMP1 gene is important in metastasis and the present study showed that Quinacrine could not affect the expression of this gene on these breast cancer cell lines.

Mycotoxin is a class of poisonous secondary metabolites generated by filamentous fungi and found in agricultural commodities worldwide. Therefore, the current study aimed to investigate how aflatoxin B1 affected hepatic cellular architecture and Matrix metalloproteinase expression in particular (MMP1 and MMP7) in the livers of experimental mice (IHC). A total of sixteen mice (four groups) were studied after being given pure aflatoxin B1 (9mg/kg B. W., 6mg/kg B. W., and 3mg/kg B. W. ) (produced from Aspergillus flavus) or a control group (not treated). MMP1 and MMP7 expressions were also measured using the MMP1 and MMP7 expression assays (IHC). The degree of liver damage is related to the AFB1 concentration and the duration of exposure. IHC reveals a considerable rise in MMP1 and MMP7 expression in the livers of mice given a maximum concentration of 90% ((9 mg/B. W. ) pure AFB1), which approached the toxin's effect toxic dosage. MMP1 and MMP7 expression were also increased by AFB1 at dosages of 60 and 30% (6mg/BW and 3mg/B. W., respectively), although not to the same extent as 90%. MMP1 was significantly more expressed than MMP7 compared to control, and AFB1 at 90, 60, and 30% concentrations caused changes in hepatic cellular architecture, organization, and liver tissue damage and dramatically increased MMP1 and MMP7 production in hepatic tissue following treatment. Increased levels of pure aflatoxin B1 will harm liver tissue and MMP1 and MMP7 expression. MMP1 was more substantially expressed than MMP7.

Background and Aim: Extensive prevalence of myocardial infraction, and an increase of 36% in total deaths due to it by 2020, and attention to the causes and methods of alternative therapy is very important. There are different ways in treating these patients that endurance training is one of them. The aim of this study was to evaluate the effect of 8 weeks of incremental endurance training on serum levels of TSP-1 and MMP-1 in male Wistar rats with myocardial infarction. Materials and Methods: In this controled experimental study with control group, 20 rats weighing 230 ± 30 g (8-week-old) were randomly divided into incremental endurance training and control, after induction of infarction with Isoproteronol (150 mg/kg). The training group performed an 8-week training session (3 sessions a week, for 20 to 50 minutes at 12 to 18 meters per minute). Then, 24 hours later, the venous blood sample was collected to evaluate serum concentrations of TSP-1 and MMP-1 and transferred to the laboratory. Independent t-test was used to analyze the data at a significant level of p <0. 05 to Graphed Pad software. Ethical Considerations: This study with research ethics code IR. IAU. ARAK. REC. 1397. 007 was approved in Research Ethics Committee of Islamic Azad University, Arak branch, Iran. Findings: The results showed that endurance training significantly increased serum MMP1 levels (p = 0. 048) in rats with myocardial infraction, while there was no significant effect (p = 0. 092) on the exercise program in serum TSP-1 levels. Conclusion: the result of this study suggests that increasing endurance training may increase MMP-1 in rats with myocardial infraction, which can play an important role in angiogenesis and replacement of capillaries.

Background and Aim: Regular aerobic exercise and stem cell therapy have shown promising effects in the management of osteoarthritis. The increased expression of nuclear factor kappa B (NF-κB) plays a significant role in joint degradation in osteoarthritis, while matrix metalloproteinase-1 (MMP1) gene expression is elevated in the joint bones of osteoarthritis patients. This study aimed to investigate the effects of aerobic exercise and stem cell injection on the expression of NF-κB and MMP1 genes in the knee cartilage of male rat models of osteoarthritis. Methods: In this experimental study, 25 male rats were randomly assigned to five groups: healthy control, osteoarthritis-induced (diseased), diseased + exercise, diseased + stem cells, and diseased + exercise + stem cells. The exercise program included 30 minutes of treadmill running at 16 meters per minute during the first week, gradually increasing to 50 minutes by the eighth week, following the principle of progressive overload. Mesenchymal stem cells were administered to the relevant groups at a dose of 1×10^6 cells per kilogram via a single injection. Forty-eight hours after the final exercise session, knee cartilage tissue was extracted, and the expression of NF-κB and MMP1 genes was evaluated using Real-Time PCR. Results: The expression of NF-κB in the osteoarthritis group was significantly higher than in the healthy control group (P=0.001). Aerobic exercise resulted in a significant reduction in NF-κB expression compared to the diseased group (P=0.043). However, stem cell treatment alone did not significantly affect the reduction of this gene expression (P=0.077). Additionally, no significant differences were found in MMP1 gene expression between the study groups (P>0.05), although the pattern of changes mirrored those observed in NF-κB expression. Conclusion: While stem cell therapy alone did not show a significant effect on gene expression modulation, regular aerobic exercise significantly reduced NF-κB expression. These findings support the potential of aerobic exercise as an effective intervention to suppress NF-κB in the management of osteoarthritis.

Aim: Due to weak diagnosis and treatment of PDAC, detection of PDAC possible biomarkers in early stage is the main aim of this study. Background: Pancreatic ductal adenocarcinoma (PDAC) is known as an exocrine cancer with a 5-year overall survival of 11%. Methods: Gene expression profiles of early stage of PDAC tissue and normal tissue are downloaded from gene expression omnibus (GEO) and evaluated via GEO2R. The significant differentially expressed genes (DEGs) are investigated via protein-protein interaction (PPI) network analysis and gene ontology. Results: Among 104 DEGs, ALB, COL1A1, COL1A2, MMP1, POSTN, PLAU, and COL3A1 were pointed out as hub nodes. “Gelatin degradation by MMP1, 2, 3, 7, 8, 9, 12, 13” group of 52 biological terms were identified as the main affected terms. Conclusion: In conclusion, ALB, MMP1, and COL1A1 genes were highlighted as possible biomarkers of early stage of PDAC. Dysfunction of extracellular matrix was identified as a main event in patients

Objective(s): This study aimed to determine the collagen type II (COL2) and SOX9 expression in interleukin growth factor (IGF-1)-induced Wharton’ s Jelly mesenchymal stem cells (WJMSCs) and the level of chondrogenic markers in co-culture IGF1-WJMSCs and IL1β-CHON002 as osteoarthritis (OA) cells model. Materials and Methods: WJMSCs were induced with IGF1 (75, 150, and 300 ng/ml) to enhance their chondrogenesis capability. The gene expression of SOX9 and COL2 was evaluated with quantitative RT-PCR. Furthermore, IGF1-WJMSCs were co-cultured with IL1β-CHON002 cells in varied ratios (1: 2, 1: 1, 2: 1). Chondrogenic markers ADAMTS1, ADAMTS5, MMP3, MMP1, and RANKL were measured with ELISA. Results: The IGF1-WJMSCs had an increased expression of COL2 and SOX9. ADAMTS1, ADAMTS5, MMP1, MMP3, and RANKL levels were decreased in the co-culture IGF1-WJMSCs and IL1β-CHON002. Conclusion: The IGF1-induced WJMSCs were capable to enhance chondrogenesis, indicated by increased expression of SOX9 and COL2 and decreased expression of ADAMTS1, ADAMTS5, MMP3, MMP1, and RANKL. These findings can be further used in the osteoarthritis treatment.