A MicroRNA Regulon that Mediates Endothelial Recruitment and Metastasis by Cancer Cells - Article Example

A microRNA Regulon that Mediates Endothelial Recruitment and Metastasis by Cancer Cells Name Institution A MicroRNA Regulon that Mediates Endothelial Recruitment and Metastasis by Cancer Cells Summary A set of human microRNAs suppress spread of breast cancer cells to lungs and bones. The microRNAs were found to suppress their autonomous cancerous phenotypes. However, the role played by non- coding RNAs in non-cell dependent cancer spread in unknown. This report reveals that endogenous miR-126 suppresses metastatic initiation and colonization (Kim, Nils, Mitsukuni and Sohail, 2012). Using a stable miR-126 and control knockdown cell injections in immunodeficient mice, various organs were assessed for metastatic colonization levels. Further, it revealed a reduced increase in tumor level and increased number of nodules compared to the controls (Kim et al., 2012). In addition, miR-126, was found to suppress cancerous endothelial density, increase perfusion and functional angiogenesis. Further, the research reveals that high recruitment capacity of endothelial cells by metastatic cells result to high breast cancer cells. Though miR-126 does not reduce adhesion of endothelial cells, it was found to reduce recruitment rate of HMVEC endothelial cells and recruitment of endothelial cells by CN34 cell and HER2-positive SkBr3 (Kim et al., 2012). When tested on breast cancer cells on endothelial recruitment inhibition ability, miR-126 expression inhibited recruitment; miR-126 suppression enhanced it while miR-126 silencing did not affect the size or density of the tumor (Kim et al., 2012). The test was carried on breast cells independent of their location. MiR-126 was found to suppress a set of eight genes. This experiment was carried out using integrative transcriptomic approach. Patients with over expression of these genes were least affected by breast cancer than those without. Of the eight genes suppressed, some of them play a role in inhibiting recruitment of endothelial cells by cancer cells. From the study done using hairpins, it was reveled that miR-126, targets three of the genes (IGFBP2, PITPNC1 and MERTK), which play a role in recruitment and colonization (Kim et al., 2012). This is because of miR-126 pathway activating IGF1R thus enhancing adhesion of the two sets of cells. IGFBP2 however counteracts this activity by inhibiting endothelial cell recruitment by MDA and CN34 Par cells and colonization (Kim et al., 2012). Over expression of PITPNC1 increased recruitment rate but was suppressed by IGFBP2. Conversely, MERTK was found to be free of IGFBP2. GAS6 inhibit recruitment by reducing the action of miR-126. However its effect is suppressed by MERTK. From all the findings of the report, endothelial cells contribute to cancer spread from the breast to other body organs but this action can be suppressed by action of miR-126. However, this report does not provide sufficient proof for the findings. Criticism The report begins with an abstract. There is no hypothesis for the study given that it should be in every research work. However, within the report, the importance of every test is explained, there is no numerical means to measure the results. The study also lacks objectives of the research, thus there is not means to determine whether the research results correlate with the objectives. There is no way to check the statistical importance of the outcome (Creswell, 2003). Furthermore, being a scientific paper, there is need for definition of terms used in the report. Definition avoids misinterpretation enhancing understanding of the paper by the readers. The author should have defined terms such as metastasis, metastatic, endothelial recruitment, angiogenesis and proliferation among others. This makes the report understandable by most readers. There is not information provided about a set of microRNAs suppressing spread of autonomous cancerous cells. Therefore, there is no background information given to support this piece of information and explain the reason for the study. In addition, the author at the beginning explains that no information is known about the role played by non-coding RNAs in non-cell autonomous cell progression. Therefore, though miR-126 suppresses progression of these cells, the role played by non-coding RNAs in progression could equally outdo miR-126 suppression. These results may be justified but not reliable for practical application without further research (Creswell, 2003). The report does not give data collection methods used in details. Selection criteria for the original sample, sample sizes used for all findings is left out. At the beginning of the report, the author used immunodeficient mice. There is no information given about the extent of immunodeficiency and selection criteria for a homogeneous sample size from the available population. In addition, the sample size is not described in terms of age and size. Thus, credibility of the results is questionable. For scientific data results to be credible, statistical findings should be presented not only graphically but statistically too (Creswell, 2003). The experiment could not be repeated. Although the author presents the method at the end of the report, information about the procedure, experimental set ups, materials and laboratory setting used is missing. Further, the report lacks consistency in the organs under study. For example, while determining the role of miR-126 in metastatic progression, colonization is studied in portal system, tail vein and intercardiac system. However, only the results of the lungs are used to draw conclusions the rest of the organs are left out. The statistical aspects of a research are left out in this product. It does not point out the dependent and independent variables. The sample size used for every experiment is not the same. Criteria for selection of the sample size were not stated. In addition, by using different sample sizes then dependent and independent variables could not be identified. Selection criteria for samples used is also left out. The test did not compare analogous units. In testing for efficiency of miR-126 to suppress cancerous cells, they tested it in different organs instead of the same organs. The test was at first intended to study spread of breast cancer cells to lungs and bones but extended the test to the brain. The report is graphically presented with the graphs well labeled on both x-axis and y-axis. Time is also well presented. However, some of the data need interpretation as what is graphically present is not what the report explains. For example, a table showing standard deviations does not explain what standard deviation is, or what conclusions are drawn from various standard deviations. In addition, graphs with the y-axis presenting photons flux ratios do not elaborate the tangible results represented. Thus, a reader may not interpret this information without a guideline. The data given for most results does not directly fit the question. For example, miR-126 was found to hold back conscription, metastatic angiogenesis and metastatic instigation and control. However, no table shows these results directly. Further, interpretation of some information in the graphs is quite hectic due to many aspects being presented in one graph. This information would have been otherwise presented in statistical figures, which are easy to interpret. The data collected largely relate to the question and answers the questions. However, some information mentioned in the report is not presented statistically. For example, interaction of miR-126 with IGFBP2 and kinase MERTK 3’ untranslated regions and coding regions of protein PITPNC1 and SHMT2 in not shown. Interestingly, while testing for expression levels of IGFBP2, MERTK and PITPNC1, an additional sample size was used. Thus, there was no evidence for some of the information. In addition, though miR-126 in the end suppresses cancerous cells, a comparison for actions of miR-126 suppression, silencing and expression should have been included. Though the conclusion focuses on some of the findings of the report, it does not give full attention to the main objective of the study which, it focused on effectiveness of miR-126 in suppressing spread and growth of breast cancer cells on the endothelium. The discussions and conclusions do not reflect other research work.. Though found, as a breakthrough to non- autonomous cell suppression, effect of non-coding RNAs, should also not be ignored. This forms a basis of further research. This research did not address any problem. It mainly focused on experimental work to prove how successful miR-126 is in suppressing cancerous cells. It neither gives a recommendation for use of miR-126 in practical cases nor recommends it for further research. In addition, it does not explain any problems encountered during the research work that could have slightly altered the results or made the research fail. The reader assumes it was all smooth research work (Creswell, 2003). Though there is a list of references at the end of this report, the author did not do in-text citation. He or she has not acknowledged work done by others used in the report. This also nullifies it as a good research (Creswell, 2003). There is no way to differentiate between the authors’s original work and work from others (Hopkins, 2000). This research leaves a lot to be approved as a research paper. Though it has scientific content, the mode of presentation is wanting. In addition, it does not clearly define a hypothesis or objectives for the study. Though procedures are not provided, the paper may be adopted for a comprehensive research on the same topic. In addition, students use it to study features of a research paper use it. References Creswell, WJ 2003, Research Design: Qualitative, Quantitative, and Mixed Method Approaches, Sage publications: New York Hopkins, GW (4/5/2000), Quantitative Research Design, Sportscience, retrieved on 20th April 2012 from: www.sportsci.org/jour/0001/wghdesign.html. Kim JP, Nils Halberg, Mitsukuni Yoshida & Sohail, FT 2012, “A microRNA Regulon that Mediates Endothelial Recruitment and Metastasis by Cancer Cells,” Research Letter, Vol. 481 no. 1 9 0 Read More