microRNAs 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.

The possibilities offered by this new type of battery would indeed be considerable. From the smartphone to the tablet, via laptop, GPS or car, all energy consuming mobile power products and requiring regular refills could benefit from the advantages of this new combination. Moreover, these batteries could also be used at much larger scale than the charging alone phones or computers and storing electricity produced by renewable sources such as wind turbines or solar and tidal power.

Stem cell research is the future of medical and biological research and remedies, and it is fascinating to watch the progression of this new and important science as it unfolds. These cells were discovered in mouse embryos in the 1980s, and are remarkable because of their potential to grow into a variety of different kinds of cells within a body. Common in fetuses, and more rare in adult animals of all kinds, stem cells can be manipulated in useful ways to repair many tissues, dividing limitlessly for therapeutic purposes. When a stem cell divides, each new cell has the potential either to remain a stem cell or to differentiate into more specialized tissue, such as nerve, pancreas, bone marrow, or unique blood components. Initially

The use of stem cells can advance drug development, knowledge of disease, patience specific disease treatment, and can bypass the limits of mouse-models for research. According to the National Institute of Health (1), stem cells are unique in the following ways: they can divide and renew themselves for long periods, they are unspecialized, and they can give rise to specialized cell types. The uniqueness of these stem cells allows for the testing of new drugs, cell-based therapies and the study of human development including cancer research. Human stem cell therapies have been used for the treatment of neurological disease in human clinical trials such as Parkinson’s disease (2), spinal cord injury (3,4) stroke (5), and

The company ‘Invivogen’ made a transfectable and simple-to-use plasmid, called psiRNA™, that allows the production of siRNAs within the cells. To transfect means to introduce foreign material into eukaryotic cells. psiRNA is an RNA polymerase III-based plasmid that produces ‘short hairpin’ RNAs (shRNAs). shRNAs are more stable than synthetic siRNAs and since they are continuously expressed within the cells rather than having to be injected into the cytoplasm, this method permits long-lasting silencing of the BLG gene.

An abnormality in this process leads to a number of problems, including cancer. MicroRNAs are a type of RNA which inhibit the expression of genes and play a vital role in the development of cancer. Of notable interest is miR-378, as it increases tumor angiogenesis and growth and also enhances the survival of these cells, by decreasing the expression of tumor suppression genes like Sufu. A study testing human cell lines found that when Sufu expression levels were high, miR-378 expression levels were low, and when Sufu levels were low, miR-378 levels were high, showcasing that the two were negatively correlated. Because repression of Sufu can lead to rampant proliferation of cells, the inhibition of Sufu is essential in order for miR-378 to promote angiogenesis and increase cell

Oncogenes were discovered in the 1960s, when it was discovered that some animal cancers such as lymphomas were caused by viruses. Some of these viruses were notable due to the simplicity of their RNA genome. These viruses only had three distinct transcription units, involved in the replication of the virus (coat proteins and reverse transcriptase etc.), and an extra gene. This was an oncogene. When oncogenes are properly functioning they are termed proto-oncogenes (Todd R, 1999). Their normal function is to control cell proliferation. These function in growth signalling pathways, and conversely to tumour suppressing cells are activated through a gain in function rather than a loss of it. This occurs in two ways, by producing more of a product, or producing a subtly different product, as a result of a mutation similar to tumour suppressor genes (Croce, 2008). Oncogenes play a particularly strong role in the development of breast cancers. Often the normal ERBB2 and other related genes are amplified in late stage neuroblastomas and rhabdomyosarcomas. ERBB2 encodes HER2 which is a member of the epidermal growth factor

Methylation, specifically hypomethylation, can incessantly activate the transcription of oncogenic microRNAs which encourage carcinogenesis (Fukushige). Methylation, specifically hypermethylation, of the genome can turn off genes that can be transcripts to make microRNAs which actively work to suppress tumors. When a microRNA suffers from mutations, the altered miRNA can promote hypermethylation of tumor-suppressor genes (Lopez). DNA methylation affects the regulation of harmful, cancer-causing and can increase the incidence of pancreatic cancer. Cancer tissues were shown to have extraordinarily higher levels of methylation than non-cancerous tissues did

MiR-21 has been found to be over expressed in 20 pancreatic carcinoma tissues and cell lines compared to normal tissue or cell lines. (15)

Many studies have explored the impact of nature and nurture on stuttering behavior, but for our project we wanted to focus on epigenetics as well as specific genes hypothesized to be related to stuttering. Epigenetics is sometimes referred to as the bridge connecting nature and nurture. Epigenetics is the study of heritable changes in gene expression that do not involve changes to the underlying DNA sequence. In other words, a change in phenotype without a change in genotype. Epigenetics is suggested to reside in methyl groups, histones, and noncoding RNA. DNA methylation can be compared to turning on a faucet, in which this process turns genes “on” and “off.” Meanwhile, histones control “how much water is flowing through the faucet, by determining how tightly or loosely the DNA is wound and “read.” Finally, non-coding RNA are functional RNA molecules that are transcribed from DNA but not translated into proteins.

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

But, in chordomas, these mutations can be the result of sporadic mutations or hereditary lines mutations. In recent research papers, microRNA-608 and microRNA-34 have been proposed as novel tumor suppressors that can function as a form of targeted therapy because they were identify to regulate the downstream signaling of affected cells and therefore the overexpression of oncogenes (EGFR, Bcl-xL, MET), which are usually overexpressed when chordoma cell proliferation found. This implicates, when microRNA-608 and microRNA-34 are functioning properly, they regulate the signaling pathway of these oncogenes by prompting cells to undergo apoptosis. However, when inactive, such oncogenes are not being regulated and therefore proliferate without a systematic control, leading to chordoma tumors. This gives us some notions on the genetic origins of the mutations that can lead to chordoma cell proliferation. In many cases chordomas are very deadly form of cancer, chordoma tumors can be effectively treated with surgery, radiotherapy and resection; but due to their location and need to preserve vital adjacent structures, chordomas have a high recurrence rate and a high risk of metastasis. Recurrence rates for chordoma tumors are above 40% with an overall survival time of around 5 years after

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).

Abstract: Increasing evidence suggests cell-to-cell communication is possible through extracellular RNAs (exRNAs). RNA (including mRNA, miRNA, or lincRNA) has, on many accounts, been found packaged inside extracellular vesicles (EVs) which may traverse through a variety of bodily fluids to be taken up by a recipient cell. The biological significance of exRNAs is largely unknown. However, preliminary studies suggest they may play a role in a variety of important biological processes, including stem cell maintenance, apoptosis, and cancer metastasis. Furthermore, there is much hope in eventually utilizing EVs as a drug delivery vector to supply damaged tissues with therapeutic RNAs. Such a system could overcome the immunological challenges associated with viral vectors. Advances in understanding the biology of exRNA transfer have been hindered by a lack of dynamic methods for detecting changes in RNA concentration in vivo. Northern blotting, microarray, and PCR based approaches are invasive, and sometimes lack sensitivity when dealing with small quantities of RNA. While evidence of their significance is growing, to date no exRNA has been shown to enter and function in a cell in vivo. To address these issues, I have been working on the development of a sensor system for detecting exogenous small RNAs. This molecular sensor will exploit the ability of microRNAs (miRNAs) to bind to, and repress, target

In the present study, we demonstrate the stimulatory roles of COX-2 and EP4 in human breast cancer progression and SLC induction via PI3K/AKT/NOTCH and WNT pathways, combining in vitro, in vivo, and in situ approaches. This work supports our previous studies, wherein we showed SLC stimulatory roles of COX-2 and EP4 in a murine breast cancer model [5]. The role of COX-2 in SLC induction has been hypothesized [42] and the roles of EP4 documented in human breast cancer cells [43]. We reported that COX-2/EP4 mediated induction of an oncogenic microRNA-526b was linked with SLC stimulation [19]. However, the mechanisms underlying COX-2/EP4 mediated SLC induction in human breast cancer remained unclear. In the present study, for the first time,