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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Esophageal squamous - cell carcinoma,Linc-ROR,Non-coding RNA,Spliced variants
- چکیده:
- چکیده انگلیسی: Objective(s): Similar characteristics of molecular pathways between cellular reprogramming events and tumorigenesis have been accentuated in recent years. Reprogramming-related transcription factors, also known as Yamanaka factors (OCT4, SOX2, KLF4, and c-MYC), are also well-known oncogenes promoting cancer initiation, progression, and cellular transformation into cancer stem cells. Long non-coding RNAs (lncRNAs) are a major class of RNA molecules with emerging roles in stem cell pluripotency, cellular reprogramming, cellular transformation, and tumorigenesis. The long intergenic non-coding RNA ROR (lincRNA-ROR, linc-ROR) acts as a regulator of cellular reprograming through sponging miR-145 that normally negatively regulates the expression of the stemness factors NANOG, OCT4, and SOX2.
Materials and Methods: Here, we employed a real-time PCR approach to determine the expression patterns of linc-ROR and its two novel spliced variants (variants 2 and 4) in esophageal squamous cell carcinoma (ESCC).
Results: The quantitative real-time RT-PCR results revealed a significant up-regulation of linc-ROR (P=0.0098) and its variants 2 (P=0.0250) and 4 (P=0.0002) in tumor samples of ESCC, compared to their matched non-tumor tissues obtained from the margin of same tumors. Our data also demonstrated a significant up-regulation of variant 4 in high-grade tumor samples, in comparison to the low-grade ones (P=0.04). Moreover, the ROC curve analysis demonstrated that the variant 4 of ROR has a potential to discriminate between tumor and non-tumor samples (AUC=0.66, P<0.05). Conclusion: Our data suggest a significant up-regulation of linc-ROR and its variants 2 and 4 in ESCC tissue samples.- انتشار مقاله: 02-08-1395
- نویسندگان: Reza Sahebi,Mahshid Malakootian,Baharak Balalaee,Alireza Shahryari,Masoud Khoshnia,Mohammad Reza Abbaszadegan,Abdolvahab Moradi,Seyed Javad Mowla
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: HPLC,Esophageal Cancer,amino acid,gluconeogenic pathway
- چکیده:
- چکیده انگلیسی: Objective: Metabolic processes in the body of people with and without esophageal cancer (EC) are significantly different. Therefore, changes in the metabolism of amino acids in the body of EC patients can lead to metabolic disorders, such as increased gluconeogenesis. The aim of this study was the comparison of the plasma levels of gluconeogenic amino acids between patients with EC and the control group. Methods: Plasma samples of 37 patients with EC who were selected before any treatment or surgery, and 37 healthy adults who did not have history of family cancer and malignant diseases were taken. Analysis of the plasma levels of amino acids including, alanine, asparagine, aspartate, glutamate, glutamine, glycine, serine, arginine, histidine, methionine, threonine, valine, tyrosine, isoleucine, phenylalanine, tryptophan was done by High Performance Liquid Chromatography (HPLC) based on reverse-phase-chromatography. Data analysis was done by SPSS-16 software. Results: In the patient group the mean age ± SD was 63±13.64 and 21 (56.8%) were male.The plasma levels of the alanine, asparagine, histidine, methionine, threonine, valine amino acids in the patients with esophageal cancer was significantly reduced and glycine was increased (p-value<0.05). Conclusion: Gluconeogenic amino acids are the main precursor of glucose synthesis in the gluconeogenesis pathway. Cancer cells need more energy to grow and multiply, and glucose is used as the main fuel for cells. Given the importance of metabolic pathways in cancer cells, more detailed studies at the molecular level can provide new insights into early detection and appropriate treatment strategies for cancer.
- انتشار مقاله: 15-02-1399
- نویسندگان: Mahsa Taherizadeh,Masoud Khoshnia,Sedigheh Shams,Zahra Hesari,Hamidreza Joshaghani
- مشاهده