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

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The paper “ A MicroRNA Regulon that Mediates Endothelial Recruitment and Metastasis by Cancer Cells” is a good example of an article on biology. A set of human microRNAs suppresses the 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 the 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 an 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 the high recruitment capacity of endothelial cells by metastatic cells results in high breast cancer cells. Though miR-126 does not reduce adhesion of endothelial cells, it was found to reduce the recruitment rate of HMVEC endothelial cells and the 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 an integrative transcriptomic approach. Patients with overexpression 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 the recruitment of endothelial cells by cancer cells. From the study done using hairpins, it was revealed 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 the miR-126 pathway activating IGF1R thus enhancing the 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).

Overexpression of PITPNC1 increased the recruitment rate but was suppressed by IGFBP2. Conversely, MERTK was found to be free of IGFBP2. GAS6 inhibits 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 the action of miR-126. However, this report does not provide sufficient proof for the findings. CriticismThe 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 are no numerical means to measure the results. The study also lacks objectives of the research, thus there is no 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).

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

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