جستجوی مقالات مرتبط با کلیدواژه « tumorigenesis » در نشریات گروه « پزشکی »

MicroRNAs (miRNAs) play pivotal roles in post-transcriptional regulation of gene expression and have emerged as crucial regulators in cancer development, progression, and metastasis. This study aimed to assess the expression profiles of miR-23, miR-223, miR-1246, and miR-150 in serum samples obtained from colorectal cancer (CRC) patients before and three months after surgery, in comparison to a healthy control group, to explore their biomarker potential.

A total of 50 blood samples were collected from patients with CRC (pre- and post-surgery), along with 50 samples from healthy controls. The relative expression levels of miR-23, miR-223, miR-1246, and miR-150 in the serum were quantified using quantitative real-time PCR.

Our findings revealed upregulated expression levels of miR-23, miR-1246, and miR-223, while miR-150 exhibited significant downregulation in the serum of CRC subjects compared to healthy controls. Receiver operating characteristic (ROC) analysis indicated that miR-23 and miR-150 could distinguish CRC cases from controls with relatively high accuracy. Moreover, three months post-surgery, miR-23, miR-1246, and miR-223 serum levels were downregulated, and miR-150 was significantly upregulated. However, no significant correlations were observed between serum levels of the studied genes and the clinical features of our patients.

The serum levels of miR-23 and miR-150 hold promise as potential biomarkers for the diagnosis and prognosis of CRC.

This study aimed to investigate functional role of long ncRNA (lncRNA) 91H in liver cancer tumorigenesis,focusing on its effect on cell proliferation, apoptosis, cell cycle progression, migration, invasion, epithelial-mesenchymaltransition (EMT) and in vivo tumor growth. In this experimental study, liver cancer tissues and cell lines were analyzed for lncRNA 91Hexpression using quantitative reverse transcription polymerase chain reaction (qRT-PCR). By employing si-RNA tosilence 91H, we aimed to gain a more in-depth understanding of its specific contributions and effects within these cells.Cell proliferation was assessed through the CCK-8 assay, while apoptosis and cell cycle progression were quantifiedusing Annexin V-FITC staining and flow cytometry, respectively. Migration and invasion capabilities of liver cancer cellswere assessed through transwell assay. EMT was assessed by analyzing protein expression levels of EMT-associatedmarkers through western blotting. In vivo effect of 91H was assessed through xenograft experiments. Significantly higher levels of lncRNA 91H were observed in the liver cancer tissues and cell lines, than thenormal cells. Silencing 91H in liver cancer cells led to a notable reduction of cell proliferation by inducing apoptosisand arresting the cell cycle. Liver cancer cells with decreased 91H expression exhibited diminished migration andinvasion abilities, suggesting a role for 91H in promoting these processes. Furthermore, 91H knockdown weakenedEMT in liver cancer cells, indicating its involvement in modulating this critical cellular transition. Furthermore, growth ofsubcutaneous xenograft tumors and weight was effectively suppressed by sh-lncRNA 91H. Our study strongly supports lncRNA 91H's role in liver cancer progression by enhancing proliferation, migration,invasion, and EMT. Targeting 91H reduced in vivo tumor growth, highlighting its potential as a therapeutic liver cancer target.These findings suggest 91H's pivotal role in liver cancer aggressiveness, opening doors for future therapeutic approaches.

Esophageal carcinoma (ESCA) is one of the most common types of cancer. ESCA accounted for the sixth leading cause of cancer-related deaths globally. Most patients are diagnosed at late stages of ESCA, with distance metastasis or chemoresistance, which leads to a poor prognosis. Previous studies demonstrated lncRNA presentation and roles in ESCA cells and patients' tissue. It has been proposed that lncRNAs can be considered a new prognostic and diagnostic biomarker in ESCA. In this study, we comprehensively explored the interaction of lncRNAs with miRNAs and mRNAs of the TCGA database and proposed a novel promising biomarker with good diagnostic and prognostic values.

The public data of RNA-seq, miR-seq, and related clinical data were downloaded from the TCGA database. Differential expression analysis was conducted by “limma” in R. GO, and KEGG signaling pathways were used for enrichments. STRING database was used for PPI analysis. CE-network was constructed by the STAR database in R. Kaplan-Meier survival analysis (log-rank test), and ROC curve analysis was used to indicate the diagnostic and prognostic values of the biomarkers.

Differentially expressed data illustrated that 45.8% of the total mRNAs in the data related to ESCA patients showed increased expression and 54.2% decreased expression. The GO and KEGG pathway analysis showed that the differentially expressed mRNAs were enriched in critical biological processes. Important protein-protein interaction hubs were identified. The ceRNA network data demonstrated critical lncRNAs essential in ESCA development, including TMEM16B-AS1, AC093010.3, SNHG3, and PVT1. The data revealed that the lncRNA WDFY3-AS2, AC108449.2, DLEU2, AC007128.1, and AP003356.1 are potential diagnostic and prognostic biomarkers in ESCA patients.

Altogether, this study demonstrates lncRNA, miRNA, and mRNA interaction and mentions regulatory networks which can be considered as a therapeutic option in ESCA. In addition, we proposed potential diagnostic and prognostic biomarkers for ESCA patients.

Solid tumor cells utilize amino acid transporters (AATs) to increase amino acid uptake in response to nutrient-insufficiency. The upregulation of AATs is therefore critical for tumor development and progression. This study identifies the upregulated AATs under amino acid deprived conditions, and further determines the clinicopathological importance of these AATs in evaluating the prognosis of patients with cancers.

In this experimental study, the Gene Expression Omnibus (GEO) datasets (GSE62673, GSE26370, GSE125782 and GSE150874) were downloaded from the NCBI website and utilized for integrated differential expression and pathway analysis v0.96, Gene Set Enrichment Analysis (GSEA), and REACTOME analyses to identify the AATs upregulated in response to amino acid deprivation. In addition, The Cancer Genome Atlas (TCGA) datasets with prognostic information were assessed and employed to evaluate the association of identified AATs with patients’ prognoses using SurvExpress analysis.

Using analysis of NCBI GEO data, this study shows that amino acid deprivation leads to the upregulation of six AAT genes; SLC3A2, SLC7A5, SLC7A1, SLC1A4, SLC7A11 and SLC1A5. GSEA and REACTOME analyses identified altered signaling in cells exposed to amino acid deprivation, such as pathways related to stress responses, the cell cycle and apoptosis. In addition, Principal Component Analysis showed these six AAT genes to be well divided into two distinct clusters in relation to TCGA tumor tissues versus normal counterparts. Finally, Log-Rank analysis confirmed the upregulation of this panel of six AAT genes is correlated with poor prognosis in patients with colorectal, esophageal, kidney and lung cancers.

The upregulation of a panel of six AATs is common in several human cancers and may provide a valuable diagnostic tool to evaluate the prognosis of patients with colorectal, esophageal, kidney and lung cancers.

Gastrointestinal cancers are among the most serious cancers. In addition to environmental factors, genetic and epigenetic factors also play a key role in the development of gastrointestinal cancers. Since many molecular pathways are involved in the development of this type of cancer, the study of the function of molecular mechanisms involved in carcinogenesis and tumorigenesis and their relationship with genes involved in this malignancy in different molecular pathways to identify biomarkers used in early detection it is of great importance. The role of the Sonic Hedgehog signaling pathway in maintaining and controlling stem cell growth and its association with genes involved in gastrointestinal cancers has been reported. In this study, the importance and relationship between the DNA methylation mechanism and genes of the Sonic Hedgehog family in carcinogenesis and tumorigenesis of gastrointestinal cancers will be investigated.

In children with lymphoblastic leukemia (ALL), cancerous metastasis to the central nervous system (CNS) is common, but there is insufficient information on this metastasis and cancer progression process. Further, the role of exosomes on cancer growth and metastasis has been the attention of many studies. Because the astrocytes involve in the blood-brain barrier and stay in contact with peripheral blood , we investigated the effect of exosomes derived Nalm6 cell line on astrocytes from human brain fetal tissue.     In this in vitro study, exosomes were isolated from the supernatant of Nalm6 cell line by centrifugation and identified by DLS, AFM and FE-SEM methods. Astrocytes were isolated from human fetal brain tissue cells and expanded and identified by GFAP antibody with immunocytochemistry. Astrocytes were treated with different concentrations of exosomes (i.e., 5, 10, 30, and 50 µg/ml),. Proliferation and migration were assessed with Trypan blue staining and scratch methods, respectively. To define tumorogensis changes in astrocytes treated by exosomes, the expression of MMP9, P53, and Cox2 genes were investigated by Real-Time PCR. According to the DLS results, the size of exosomes was about 43 nm. AFM and FE-SEM imaging indicated these exosomes have a spherical shape. Our results showed that the proliferation of astrocytes significantly increased when treated with 50 µg/ml of exosomes.Therefore, the concentration of 50 µg/ml was considered for further experiments. Astrocyte migration was significantly increased compared to the control group. Finally, our results showed tumorogenesis changes in astrocytes by increasing the expression of MMP9 and Cox2 and decreasing the expression of p53 at mRNA level. Based on our in vitro study, exosomes derived from ALL as a peripheral tumor can change the behavior of astrocytes as a target for metastasis. Further investigations on this topic are warranted to shed light on metastatic mechanisms.

Mitochondria implement various cellular functions, including energy production through the electron transport chain by oxidative phosphorylation mechanism. These respiratory chains consist of several complexes and protein subunits which are encoded by nucl ear and mitochondrial genes. Due to mutation susceptibility and repair limitation, more aberrations have occurred in mitochondrial DNA in comparison to nuclear DNA. Given the fact that mitochondrial DNA lacks introns, mutations almost occur in the coding s equence, which comprises a direct impact on its functions. Emerging evidence indicates that mutations in the mitochondrial DNA led to the production of reactive oxygen species, disrupted apoptosis, and tumor development. Studies reported various somatic a nd germline variants in mitochondrial DNA related to tumorigenesis. The D - loop region which is the starting point for replication and transcription of mitochondrial DNA is the most prevalent site of somatic mutations in solid tumors. The D - loop mutations a lso cause copy number variations which are gaining interest in studies of solid tumors including breast cancer, colon cancer, hepatocellular carcinomas, and prostate cancer. Most studies have reported a mitochondrial DNA reduction which subsequently preven ts apoptosis and promotes metastasis. The mitochondrial DNA region - specific haplogroups are also involved in the sequence variations due to processes such as genetic drift and adaptive selection. This review article discusses the biology and function of mi tochondria and related genes. By explanation of mitochondrial dysfunction caused by different kinds of alterations, we attempt to elucidate the role of mitochondria in tumorigenesis. Prominently published articles in this field were reviewed and the role o f germline and somatic mutations of mitochondrial DNA have been investigated in common cancers.

Neuroblastoma, oneof themostprevalent infant malignancies, is heterogeneousandeasily spreads into other organs causing life-threatening consequences. Different characters of organs (such as the germ layers where the organs derived from) exert different growth microenvironments and potentially influence the behavior of metastatic neuroblastoma cells and the prognosis of patients. However, limited information is been known about this in neuroblastoma. To compare characteristics of neuroblastoma, primarily originating from the same germ layer (the seeds), in different tissues (microenvironment) derived from different germ layers. We performed retrospective analysis of SEER (Surveillance, Epidemiology, and End Results) data (1973 - 2014), patients with malignant neuroblastoma were grouped basedonthe primary lesion site (mesoderm-, ectoderm- or endoderm-derived tissue). Baseline demographic and clinical characteristics were compared between groups. Due to difficulties of processing incomplete SEER data, therapeutic method and survival rates were analyzed using cases from another SEER database (2000 - 2014). The analysis included 3701 patients: 1970 (53.2%) in themesodermgroup, 1017 (27.5%) in the ectoderm groupand714 (19.3%) in the endoderm group. Tumor histology differed between groups (P < 0.01): the ectoderm group had mostly neuroblastoma (79.2%), as did the mesoderm group (71.1%), whereas the endoderm group contained mainly olfactory neuroblastoma (94.7%). The tumors (mean size: 69.14  58.37 mm) were most commonly poorly differentiated with local extension, although lymph node invasion and distant metastasis occurred in a minority of cases. Compared with the other groups, the endoderm group had smaller (43.89  20.84 mm) and better-differentiated tumors and a lower prevalence of lymph node invasion and metastasis (P < 0.05). Despite this, overall survival was poorest for the endoderm group (P < 0.05). Radiotherapy improved overall survival in the endoderm and ectoderm groups but worsened overall survival in the mesoderm group (P < 0.05). Malignant neuroblastoma characteristics may be influenced by the tumor microenvironment. In the youngest patients, decision-making regarding the best choice of therapy should be delayed until accurate risk stratification is possible.

One of the negative effects of ionizing radiation is the alteration of cellular signaling pathways which lead to carcinogenesis and tumorigenesis. In this review, we discussed the impacts of ionizing radiation on cells and cellular signaling pathways. In this regard, exposure to radiation can directly or indirectly alter cellular signaling pathways. Remarkably, irradiated cells release special mediators into cellular matrix, aberrating cell-cell and cell-environment interactions. Most notably, these mediators include nitric oxide (NO), reactive oxygen species (ROS), and cell growth factors which contribute to cellular interactions between irradiated cells and their neighbor cells, a phenomenon known as radiation-induced bystander effect. DNA molecule is the most important cellular compartment damaged by ionizing radiation. On the other hand, the ability of irradiated cells to repair the damaged DNA is very low. Therefore, DNA alternations are passed to the next generations, and ultimately lead to carcinogenesis. The study of ionizing radiations and their impacts on biological systems is of remarkable importance to divulge their impacts on cellular signaling pathways.

Accumulating evidence suggests that self-renewal and differentiation capabilities reside only in a subpopulation of tumor cells, termed cancer stem cells (CSCs), whereas the remaining tumor cell population lacks the ability to initiate tumor development or support continued tumor growth. In head and neck squamous cell carcinoma (HNSCC), as with other malignancies, CSCs have been increasingly shown to have an integral role in tumor initiation, disease progression, metastasis, and treatment resistance. In this article, the author summarizes the current knowledge of the role of CSCs in HNSCC and discusses the therapeutic implications and future directions of this field.