The Role Of Micrornas In Cancer

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

Two predominant genes that contribute to cancer are tumor suppressor genes or oncogenes. The gene known as p53, is also called TP53 or the tumor protein. This gene helps proteins

A gene that encodes for a protein to function as a tumor suppressor as well as to regulate the cell cycle are called p53, TP 53 or tumor protein. A mature p53 mRNA is found to be 2.2-2.5 kb in size and can be found mostly in the spleen and thymus, this gene is separated by 10 introns and are split into 11 exons. As said in the chapter one of the “p53 suppressor genes” book, the final product of the p53 genome was first identified as an antigen that bound to a simian virus T antigen and adenovirus E1B oncoproteins. (Mukhopadhyay, Maxwell & Roth 1995). Mutations, deletion, insertion or rearrangement of this gene p53 which changes the biochemical and the biophysical properties is strongly associated with an increase to cancer as the article “p53 in health and disease” describes. (Vousden & Lane 2007). The mutated genes are called oncogenes, where the DNA is altered from its original form. These gene help in growth regulation and division of the cells and are often causes the cells to divide out of control causing cancer to develop from the mutations of the gene p53.

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

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,

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,

1) Downregulation of miRNA processing enzymes, such as a) Drosha by inducing expression of the oncogenic transcription factor c MYC or

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.

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.

For cancer to develop, a single cell in the body must be mutated so that it undergoes continuous and uncontrollable cell division without the ability to exhibit apoptosis (i.e. programmed cell death for the good of the organism). In order to gain these abilities, a series of genes must mutate simultaneously within the cell. First, a class of genes called oncogenes must be turned on to express themselves at high levels. Activation causes the loss of apoptosis ability and accelerates cell growth and cell division. In addition, another class of

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.

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.

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.

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