The Role Of Micrornas In Cancer

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.

Depletion of miR-142 in Ago2 profile, compared to total cellular profile and down regulation of miR-142 in EBV infected, was a clear indication of downregulation of miR-142 as atumor suppressor in DLBCL. It has been shown that miR-142 downregulated in many type of cancers and such low level of mir-142 represent a poor outcome . In our group, we have shown that 20% of miR142 harbor a point mutation at seed region and those point mutation results, in loss of tumor suppressor activity [41] . Here we propose

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

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

Several features in cancer-stromal interaction may serve as clues for studying R&R mechanism. First, small nucleotide elements with transformation potential can be packed in exosome vesicles (EVs) of 30-150 nm in size and transmitted between cells (REF). Since we have found that certain CTCs produce large amount of EVs (REF), these exosomes may transmit nucleotide regulatory elements, mostly in the form of non-coding RNAs (ncRNAs) such as microRNA (miRNA), to cause neighboring bystander cell transformation (REF). Second, we

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,

miRNAs (onco-miRs) may act as oncogenes expressing high levels in some cancers and Some miRNA act as tumor suppressor genes which are weakly expressed or even absent in tumors. They act by allowing the expression of oncogenes.

Since the discovery of miRNA by Victor Ambros, the function of miRNAs in developmental timing in C. elegans, was extended to the association of miRNAs with cancer. We now know that miRNAs can act as oncogenes (oncomiRs), by inducing different mechanism such as cell proliferation, migration and invasion, tumor growth and metastasis, or act as a tumor suppressors by inhibiting cell proliferation, migration and invasion [52]. The most common molecular genetic changes in miRNA expression level or genetic abnormality, which will be discussed below have been found to be linked to numerous cancers as follows:

Gastrointestinal (GI) cancers, such as colon and pancreas are highly resistant to both standard and targeted therapeutics. Therapy-resistant and heterogeneous GI cancers harbor highly complex signaling networks (Resistome) that resist apoptotic programming. Commonly used Gemcitabine (GEM) or platinum-based regimens fails to induce perturbations in the resistome, resulting in high rate of treatment failure. GI cancer resistance networks are in part due to interactions between parallel signaling and aberrantly expressed microRNAs (miRNAs) that collectively promote the development and survival of drug-resistant cancer stem cells (CSCs) with epithelial-to-mesenchymal transition (EMT) characteristics. The lack of understanding of

It has been reported in lung cancer tissues and cell line MIRL lncRNA acts as an oncogene. This downregulation is confirmed by knocking down MIR4435-2HG in lung cancer and treating the lung cancer cells with resveratrol. In both the cases,

The mouse model for TBI was successfully constructed. The MSCs exhibited a small round shape after fresh separation. After being cultivated and passaged, the MSCs were homogeneous and fusiform shaped. After identification by FACS, the positive ratios of CD45, CD34, Sca-1 and CD90, were 0.96%, 0.75%, 99.42% and 98.01%, respectively, thus most cells were CD45(-), CD34(-), Sca-1(+)and CD90(+) (Fig.1). RNA extracted from the MSCs was qualified and then used in circRNA microarray analysis.

Invasions result in the destruction of healthy tissue among one’s central physique. Moreover, such invasive cells may even allow for the generation of capillary blood vessels from those that are existing as a source for their survival through the process of angiogenesis. The tissue and/or organ in which the tumor has derived from or originated allows for cancer classification and characterization. Derived from epithelial cells, carcinomas exist to be one of the most common forms of cancer that lead to mortality. For instance, the primary tumor that arises among the breast is also known as breast cancer, while metastatic cells derived from the female reproductive organ would be classified as gynecologic/ovarian cancer. Rather than by mere unfortunate chance, the metastasis of tumor cells is conceived by way of its growth environment and cell interactions. Among the most prevalent cancer incidences amidst women, these forbidding diseases arise typically on account of inherited genetic mutations [in BRCA1/BRCA2], as well as through the inevitable process of aging.

tumors. 6 Mirkin and co-worker’s objective was to develop a SNA that could simultaneously regulate

Quantitative RT-PCR results show that expression levels of miR-206 are obviously lower in TNBC cell lines than those in non-TNBC cell lines (Fig. 1A). Similarly, TNBC tissues express prominently lower levels of miR-206 compared to non-TNBC tissue samples and normal breast tissues (Fig. 1B). It is worth noting that non-TNBC tissues expressed lower miR-206 compared to normal breast tissues but miR-206 levels in non-TNBC tissues were higher than those in TNBC tissues (Fig. 1B). Furthermore, we analyzed the expression levels of VEGF protein determined by immunohistochemical staining in breast cancer tissue samples. VEGF expression levels were inversely correlated with those of miR-206 in breast cancer tissues (Fig. 1C). These results demonstrate that expression levels of miR-206 are predominantly downregulated in TNBC tissues in comparison to non-TNBC tissues and normal breast tissue samples inversely correlated with the levels of VEGF.

This is the first study of its kind, with a comprehensive analysis of the prognostic effects of miRNA in stage II colorectal cancer in the form of a systematic review and meta-analysis.