Showing 4 results for Lncrna
Sajjad Cheraghi, Hamid Asadzadeh Aghdaie,
Volume 14, Issue 1 (3-2023)
Abstract
ntroduction: Colorectal cancer (CRC) is one of the most important cancers and the second leading cause of cancer mortality in Iran. CRC is spread through genetic and epigenetic changes. Understanding the molecular pathways in these genetic and epigenetic changes can provide a clear perspective on cancer treatment.
Materials and Methods: This study was performed on 40 samples of intestinal tumor growths (polyps), 30 tumor samples and 40 normal tissues adjacent to the tumor. RNA and tissue DNA extraction, study of gene expression, miR-22, miR-194 LncRNA MINCR using Real time PCR was performed.
Results: In this study, the expression of MINCR LncRNA in tumor and polyp samples increased compared to the adjacent normal tissue and the expression of miR-194 miR-22 was decreased. Negative correlation coefficient was observed between miR-22, miR-194 and MINCR expression levels and also a significant relationship was observed between the expression of these lncRNAs and microRNAs.
Volume 17, Issue 3 (10-2014)
Abstract
Objectives: Long non-coding RNAs (lncRNAs), a vast class of recently discovered non-coding genes in the human genome, have been implicated in the regulation of several biological processes, including the maintenance of stem cell pluripotency and neurogenesis. New evidences have emerged that some long IncRNAs act as enhancers for their neighboring genes. Oct4, also known as POU5F1 and Oct3/4, functions as a master regulator in maintaining the properties of pluripotency and self-renewal of embryonic stem (ES) cells and embryonal carcinoma (EC) cells. Oct-4 expression must be tightly regulated; too much or too little expression can lead to cell differentiation. Methods: PSORS1C3, an IncRNA, is located upstream of the Oct4 gene. This IncRNA could potentially impact the level of Oct4 expression. Here, we have investigated potential expression of PSORS1C3 on 23 different human pluripotent and cancer cell lines by means of RT-PCR. Results: Our results revealed a noticeable expression of PSORS1C3 both in a well-known pluripotent cell line (NTera2/NT2) and five different cancer cell lines (AGS, 5637, Ht-29, HepG2 and PC3). Conclusion: We detected the expression of PSORS1C3 for the first time in both cancer cell lines and stem cells.
Volume 22, Issue 4 (10-2019)
Abstract
Aims: The combined therapy of cancer is more effective than using a single drug to treat. In the present study, the anticancer effects of doxorubicin and doxorubicin in combination with zinc oxide nanoparticles on the MCF-7 breast cancer cells were investigated.
Materials & Methods: MCF-7 cells were cultured in RPMI1640 medium. The number of viable cells and the activity of mitochondrial dehydrogenase enzyme were evaluated by MTT assay for 24, 48, and 72 hours and IC50 was determined. RNA was extracted and then cDNA was synthesized. Specific primers for the INXS and TBP genes were designed using proprietary software. The expression level of INXS gene compared with TBP reference gene using Real-Time PCR method was assessed.
Findings: The expression of the INXS gene in doxorubicin-treated MCF-7 cells at 24, 48, and 72 hours was 7.93, 1.71, and 0.19, respectively, and in doxorubicin-treated cells with zinc oxide nanoparticles was changed 1.81, 6.34, and 15.96 at 24, 48, and 72 hours, respectively.
Conclusion: Simultaneous treatment with doxorubicin and zinc oxide nanoparticles at low concentrations (3.125 and 6.25) can cause more cell death than doxorubicin treatment alone. This may be due to the facilitation of doxorubicin entry into the cell in the presence of zinc oxide nanoparticles.
Volume 26, Issue 1 (11-2023)
Abstract
Introduction: Statins are one of the approved drugs used in the clinic, which are prescribed to reduce the amount of cholesterol in the blood of patients. However, the effects of the drug in reducing the amount of fat and the occurrence of side effects are not the same in the patients. Considering the role of LncRNAs in regulating gene expression, the possible role of HOTAIR LncRNA and atorvastatin treatment in regulating HMGCR gene expression as the main regulating gene in cholesterol synthesis has been investigated.
Methods: Bioinformatics analyses were used to find common regulatory factors between the HMGCR gene and candidate LncRNAs. MTT assay was used to determine the optimal dose of atorvastatin treatment on the HepG2 cell line. RNA extraction, cDNA synthesis, and quantitative analysis of gene expression were performed by qPCR. Finally, HMGCR protein expression was evaluated via the Western blot technique.
Results: Bioinformatic analyses showed that there is a relationship between HMGCR expression and some LncRNAs (HOTAIR, TUG1, MALAT1, GAS5, JPX, DLX6AS). In the cell culture, atorvastatin treatment increased the expression of HMGCR at mRNA and protein levels in the HepG2 cell line. Among the candidate lncRNAs, HOTAIR LncRNA expression decreased by 80% under atorvastatin treatment. Downregulating of the HOTAIR gene led to increased HMGCR gene expression at the RNA and protein levels.
Conclusion: The results of this study indicated that, aside from blocking the HMGCR enzyme binding site, atorvastatin can regulate the expression of HMGCR mRNA and protein by changing the HOTAIR expression.
