Lncrna Essay

3- (30 pts) miRNAs, which are a class of small RNAs, can function as oncogenes or tumor suppressors in cancer. Explain one disease, other than cancer, that can be associated with miRNAs or other small RNAs.

Aim 2 is to test the hypothesis that exRNA produced by Cn during host infection of the CNS is a detectable molecular biomarker for cryptococcal infection.

Today we will be focusing the genes that cause Lung Cancer. There are actually multiple genes that can lead to lung cancer, however, one of the most common ones is the EGFR gene. The EGFR gene is going to be the gene we are going to talk about today. I know we are getting very narrow, but after all, I have four minutes to explain the cure for lung cancer. It is just to0 vast of a subject. That is why we are going into detail for a specific area of lung cancer. This is all about targeted Therapy. So what is this EGFR gene. EGFR stands for Epidermal growth factor receptor. It is composed of C22H23N3O4. It has a molar mass of 393.436 g/mol. It is located on Chromosome 7 of our cells, with a specific position of 7p11.2. It is responsible for controlling the rate in which cells grow and divide. When this gene is turned on, it signals cells to grow and divide. When it is turned off, cells do not grow and divide. It is programmed to turn and off at a consistent rate. When this gene is born wrong, mutated, or damaged, it constantly turns on. This causes cells to grow and divide at rapid rates without dying. These cells that grow are cancer cells. As more and more of these cells grow, it forms a tumor. We already know what those

The functions of telomeres includes protection of chromosomes from degradation and end to end fusions, maintains the stability of chromosomes, acts as a mitotic clock to understand the replicative history of a cell.Telomerase is a ribonucleoprotein DNA polymerase that helps in maintaining the telomeres by adding TTAGGG repeats at the ends of chromosomes (Greider and Blackburn,1989). Telomerase consists of two main subunits: telomerase RNA (hTR) and catalytic component human telomerase reverse transcriptase (hTERT). The enzymatic activity is usually absent in somatic cells but remains active in germ line cells,embryonic stem cells and tumor cells. Almost 80 to 90% of human cancers are characterized by the presence of telomerase activity.Studies on glioma shown that more than 50% of tumors have telomerase activity and its detection rate increases with the grades of malignancy (Tchirkov et al 2003). Therefore knockdown of hTERT expression may help in the development of novel therapeutic strategies. In the present study we evaluate the effect of siRNA to downregulate hTERT in LN18 cells and also investigated the effect on apoptosis and cell

Under normal conditions, cells balance division and apoptosis, and these processes are accomplished and preserved by several biochemical “checkpoints” during the cell cycle2. When these checkpoints are affected, uncontrolled cellular proliferation and cancer can result. Two general classes of cancer genes are oncogenes and tumor suppressor genes. Oncogenes facilitate tumor formation by directly accelerating cell division, whereas tumor suppressor genes, when affected, allow uncontrolled growth that was normally suppressed2. Tumor suppressor gene loss usually affects a cell’s phenotype when both copies of the gene are lost, so null alleles can be present in a heterozygous state in cells without affecting cell and tissue phenotype. The loss of these genes can occur through genetic mutation or the epigenetic silencing of genes via promoter

From my studies, I have been able to demonstrate several links between lung cancer and smoking. It is indeed scientifically proven, that smoking is one of few factors that develop lung cancer – in fact it is the greatest. There are several pieces of evidence that support this theory, and are included later in this report.

Lung cancer is the leading cause of cancer-related deaths in the United States and worldwide 1 [1]. The survival rate of lung cancer patients is markedly improved in recent years due to development of the lung cancer screening program and targeted therapy. It is well-known that the development and progression of lung cancers, including both small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC), are multi-step process. The GCTA data have shown that several oncogenes, such as AKT1, Anaplastic lymphoma kinase receptor (ALK), Epidermal Growth Factor Receptor (EGFR), ERBB2, Kirsten rat sarcoma viral oncogene (KRAS), MET, NRAS, BRAF, PIK3CA, RET, ROS1, and others are involved 2,3,4,5,6,7[2-7]. Based on these emerging data, many

Breast cancer is the second most common cancer in women worldwide. The most common type of breast cancer is ductal carcinoma, which arises in cells that lines breast duct. Many imaging techniques are used for the screening and diagnosis, but typically patients are diagnosed at advanced stage only, and the prognosis is associated with early detection. At present serum and protein biomarkers improving early detection of breast cancer, these make better treatment options with a better response. MicroRNAs and CA 15-3 most widely used serum biomarker in breast cancer. Amplification of chromosomal regions encoding oncogenic miRNAs is consequently silencing or inhibits tumor suppressor genes. The standard treatment options for breast

In about a third of primary ovarian tumour, EEF1A2 is raised in copy number, and whilst EEF1A2 mRNA is not measurable in normal ovarian epithelium, the rate of EEF1A2 mRNA is increased in a third of ovarian tumours. It appears here that EEF1A2 is an important ovarian cancer oncogene (Lee, 2003). Moreover, when the eEF1A2 expression is induced in human ovarian cell line, the eEF1A2 expressing cell line is more tumorigenic; this proves that eEF1A2 promotes malignancy in ovarian cells (Anand et al., 2002). EEF1A2 is also an oncogene in lung adenocarcinoma (Li et al., 2006). And in a high proportion of pancreatic carcinoma, eEF1A2 is up-regulated while it is just a little bit expressed in normal pancreas (Cao et al., 2009). EEF1A2 over-expression seems to enhance cell growth, proliferation, motility, survival and invasion of pancreatic cancer cells (Cao et al., 2009). In two third of breast cancer, EEF1A2 is over-expressed, which indicates that eEF1A2 might be an oncoprotein (Tomlinson et al., 2005). But interestingly, it has been shown that eEF1A2 also augurs

MicroRNAs are short non-coding RNAs play main role in human diseases; it deregulates the RNA and represses the translation process by controlling gene expression. Some deregulated miRNAs express deferentially such as mir-125b, mir-145, mir-155, and mir-21 leads for partition between cancer and normal tissues. miRNAs expression with particular cancer biopathologic features in breast, such as tumor stage, estrogen and progesterone receptor expression, vascular invasion, or proliferation index. Exiqon microarrays analysis revealed that the most of the miRNAs down regulated in hereditary breast cancer by comparing the normal and cancer tissues, and by using mechanism of tumor progression and also pathway enrichment analysis showed

JAK2/STAT signaling pathway was one of the most significantly differentially expressed gene sets in BC compared with CP progenitors. This signaling pathway increases the ADAR1 expression in progenitor LSCs and promotes ADAR1-mediated A-to-I editing. Furthermore, ADAR1 impairs biogenesis of tumour suppressive miRNAs, thereby contributing to cancer progression. Since the let-7 miRNA family is also related to self renewal of LSC, it led the authors to investigate the correlation between JAK2/STAT pathway and LIN28B/let-7-axis, they hypothesized that the LIN28B/let-7self-renewal axis may also be disrupted by increased JAK2 signaling. This hypothesis was validated by a lentiviral transduction of BCR-ABL1 in normal progenitor, it shows an

Cardiovascular disease (CVD) is the major macrovascular complication of diabetes mellitus as well as the main cause of death from clinical observation. There are about 75% of patients with type 2 diabetes have died of myocardial infarction as reported. Non-coding RNA (ncRNA) is an RNA molecule that is not translated into a protein, which include snoRNAs, microRNAs, siRNAs, piRNAs, lncRNAs and others. Recently, increasing number of evidences implicate that these ncRNAs are crucially involved in many cellular responses as well as physiological and pathological processes of several diseases. In this review, we summarize recent progress in research on functional regulatory of series of ncRNAs in cardiovascular disease with Diabetes Mellitus. Meanwhile,

It may be possible to correct an abnormality in a tumor suppressor gene such as P53 by inserting a copy of the wild-type gene; in fact, insertion of the wild-type P53 gene into P53-deficient tumor cells has been shown to result in the death of tumor cells (3). This has significant implications, since P53 alterations are the most common genetic abnormalities in human cancers. The over expression of an oncogene such as K-RAS can be blocked at the genetic level by integration of an antisense gene whose transcript binds specifically to the oncogene RNA, disabling its capacity to produce protein. Experiments in vitro and in vivo have demonstrated that when an antisense K-RAS vector is integrated into lung cancer cells that over express K-RAS their tumorigenicity is decreased (4).

1.2 Long non-coding RNAs Although the heterogeneous group of long non-coding RNAs (lncRNAs) account with approx. 80 % for the majority of ncRNAs in the mammalian transcriptome (Kapranov 2007), miRNAs have been in the main focus of ncRNA research in the last years. However, there is recent increase in publications describing key functions of lncRNAs in central biological processes (Taft et al. 2010) and diseases.

JAK2/STAT signaling pathway was one of most significantly differentially expressed gene sets in BC compared with CP progenitors. This signaling pathway increases the ADAR1 expression in progenitor LSCs and promotes ADAR1-mediated A-to-I editing. Furthermore, ADAR1 impairs biogenesis of tumour suppressive miRNAs, thereby contributing to cancer progression. Since the let-7 miRNA family is also related to self renewal of LSC, it led the authors to investigate the correlation between JAK2/STAT pathway and LIN28B/let-7-axis, they hypothesized that the LIN28B/let-7self-renewal axis may also be disrupted by increased JAK2 signaling. This hypothesis was validated by a lentiviral transduction of BCR-ABL1 in normal progenitor, it shows an increase