Background: We started with RNA-seq analysis and aimed to investigate the possibility of secretory protein matrix metalloproteinase-3(MMP3) as a new diagnosis and therapeutic target in cervical cancer. Methods: The study was conducted on Nov 2021 at the Second Affiliated Hospital of Qiqihar Medical University, Qiqihar, China. Through conjoint analysis of gene expression data as well as survival rate data, we explored the potential secretary proteins associated with cervical cancer carcinogenesis. One hundred patients aged 38-72 years with clinical stage I-IV cervical cancer, and 100 age-matched healthy women were included. The expression changes in serum of clinical patients was detected. We knockdown or overexpressed the secretory proteins then explored its influence on biological function of cervical cancer cells. Results: By cross-analysis of The Cancer Genome Atlas (TCGA) database and MetazSecKB database, MMP3 gene was most significantly upregulated in cervical cancer patients (P < 0.05). Furthermore, MMP3 protein was remarkably increased in the serum of clinical cervical cancer patients and decreased after receiving treatment. Overexpression of MMP3 in HT-3 cells or culturing new cells using the supernatant of the medium after MMP3 overexpression could increase cell viability (P < 0.05) as well as proliferation (P < 0.05). Knockdown of MMP3 reduced the phosphorylation of PI3K as well as AKT proteins, while the PI3K phosphorylation inhibitors could suppress the impact of MMP3 on increasing cell proliferation as well as viability. Conclusion: MMP3 could be an underlying target for early diagnosis and treat cervical cancer in the future.

Background: Endometriosis is identified as presence of the endometrium outside the uterine cavity. Retrograde menstruation contributes to the endometrial tissue implantation and the establishment of endometriotic lesions at ectopic sites. It has been suggested that the endometriotic lesions are rich in angiogenic growth factors, while they have an essential role in survival and invasion of these cells. We investigated regulation of microRNA-93 (miR-93) and its involvement with vascular endothelial growth factor A (VEGFA) and matrix metalloproteinase (MMP) 3 expression in women with endometriosis. Materials and Methods: This was a cross-sectional study at Central Surgical Installation, Dr. Cipto Mangunkusumo General Hospital, Jakarta, Indonesia, between October 2020 and November 2021. Eutopic and ectopic endometrial tissues were collected from 30 subjects with laparoscopically-confirmed endometriotic women. Normal endometrial cells of non-endometriosis women served as controls. Total RNA was isolated from all samples and a quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was used to analyze the expression of miR-93, VEGFA and MMP3. Results: There was no significant difference in the expression levels of VEGFA (2. 14 ±,0. 50, P=0. 719) and MMP3 (2. 99 ±,0. 42, P=0. 583) between endometriotic lesions of endometriosis women and the healthy endometrium. Expression of miR-93 was significantly lower in the eutopic endometrium (16. 7 fold) and ectopic endometriotic lesion (20 fold) compared to the normal endometrium (P<0. 001). Furthermore, we also observed a significant correlation between miR-93 and VEGFA expression in eutopic endometrium obtained from women with endometriosis (r=-0. 544, P=0. 029). Expression of the miR-93 was also negatively correlated with MMP3 expression in both eutopic (r=-0. 412, P=0. 01) and ectopic (r=-0. 539, P=0. 03) endometrial cells of women with endometriosis. Conclusion: VEGFA and MMP3 expression levels trended to be increased in both eutopic and ectopic endometrial tissues of endometriosis women, while down-regulation of miR-93 might be involved in the alteration of VEGFA and MMP3 in endometriosis.

Introduction: Breast cancer is the most common malignancy in Iranian women. Nevertheless develops in breast cancer diagnosis and treatment, some patients die from metastasis. Matrix metalloproteinase enzymes have important role in mammary gland evaluation and production. These enzymes degrade different components of extra cellular matrix. Matrix metalloproteinase-3 (MMP-3) is one of the most important members of MMPs family. Also MMP3 affect on mammary gland evaluation. There is a single adenine insertion/ deletion polymorphism (5A/6A) at the position -1171 MMP3 gene promoter. This polymorphism affect on MMP3 expression, so the 5A allele express more than 6A allele. As a result of this SNP and MMP3 over expression, malignant tumors are created.Material and methods: MMP3 genotyping was done with PCR-RFLP technique on 120 cancer patients and 60 controls. The breast cancer patients were divided in to two groups: metastatic patients (M+) and non- metastatic patients (M-).Results: The results show that the 5A allele was more prevalent in the M+ group than controls and M- (OR= 2.91, P= 0.74, 0.94-8.98 CI 95%).Conclusion: So the probability of metastasis increase in 5A/5A genotypes.

Introduction: Lichen planus is an inflammatory chronic illness with unknown cause that can irritate the oral mucosa. P53 is associated with malignant changes in oral epithelial cells. MMPs can destroy intercellular junctions and cause acantholysis. It seems that MMP-3 plays a significant role in this regard. The purpose of this study was to evaluate the salivary levels of P53 and MMP-3 in the patients with Oral Lichen planus (OLP) compared with the control group. Materials and Methods: 30 salivary samples were collected from patients with OLP (15 with erosive Oral Lichen planus (EOLP) and 15 with reticular Oral Lichen planus (ROLP)) and 30 salivary samples from healthy people as a control group. The salivary P53 and MMP-3 level was assayed by ELISA method. Statistical analysis of the Student’ s t-test, ANOVA and Pearson correlation coefficient was performed. Results: The salivary concentrations of P53 and MMP-3 in patients with EOLP were significantly higher than patients with ROLP and control group, but no significant difference was found between control group and patients with ROLP. Conclusion: The salivary concentrations of P53 and MMP-3 were significantly different between different clinical types of OLP.

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.

Background: Osteoarthritis (OA) is a chronic disease that attacks joints and bones which can be caused by trauma or other joint diseases. Stem cell and Conditioned Medium (CM) of stem cells are developed for OA therapy, which is minimally invasive. It can decrease inflammation and be a replacement for knee surgery. This study aimed to utilize human Wharton’ s Jelly-Mesenchymal Stem Cells (hWJMSCs) as an alternative OA therapy. Methods: CM from hWJMSCs induced by IGF1 was collected. The OA cells model (IL1β-CHON002) culture was treated as follows: 1) with hWJMSCs-CM 15% (v/v); 2) with hWJMSCs-CM 30% (v/v); 3) with IGF1-hWJMSCs (IGF1-hWJMSCs-CM) 15% (v/v); 4) with IGF1-hWJMSCs-CM 30% (v/v). Parameters including inflammatory cytokines (IL10 and TNFα ), extracellular matrix degradation (MMP3 expression), and chondrogenic marker (COL2 expression) were determined. Results: The most significant increase in COL2 chondrogenic markers was found in IL1β-CHON002 treatment using 15% CM of hWJMSCs induced with IGF1. CM of hWJMSCs can reduce inflammatory cytokines (TNFα and IL10) and matrix degradation mediator MMP3. Better result was gained from IGF1-induced hWJMSCs-CM. Conclusion: CM of IGF1-hWJMSCs reduce inflammation while repairing injured joint in the human chondrocyte OA model.