Understanding Breast Cancer - Essay Example

? Understanding Breast Cancer. Understanding Breast Cancer. Introduction With ever increasing scientific research, one wonders why cures for certain diseases remains unknown. Breast cancer is one of the known cancer diseases whose cure remains speculative. Though, doctors and researchers have always been blamed for not doing much to ascertain the real treatment of breast cancer, the lack of basic information about the disease has increased its spread. It is well understood that not everybody is a scientist. What is never mentioned, however, is that everybody has the right to read and get the most basic information about any disease including breast cancer. This news brief seeks to inform everyone that breast cancer is real, and with ever increasing research, the root cause hence the cure for the diases shall be known. Since it was rerpoted that breast cancer exists, a number of studies have sought to understand the its real cure. In most recent studies, it has been indicated that KLf8 to MMP14 signaling is the principle facilitator of metastasis of breast cancer (Lu et al, 2013). According to Lu et al KLf8 to MMP14 signaling helps in progression of breast cancer in human. Lu et al hinted that KLF8 also called the Kruppel-like factor 8, plays a significant role in regulating critical transcription gene, which is a gen responsible for causing cancer. However, what remains unclear is the conditions and mechanism of the operation of this gene. According to Lu et al, KLF8 facilitates the activity, rather than the matrix metalloproteinase expression. Background. The debate on the cause and treatment of breast cancer has never ceased. There is lacking scientific proof that breast care can be cured. The number of studies that have sought to ascertain the real cause of this deadly disease has always increased (Ara, & Deyama, 2000; Cristofanilli, 2006). However, most were focused on the initial stages of breast cancer. According to Nawrocki-Raby and Gilles (2003) metastatic cell can help increase the survival chances of a breast cancer patient. Symowicz and Adley (2007) noted that Kruppel-like factor 8 an important cancer promoting protein occurs in different categories of cancers. Zhao and Reiske (1998) KLF8 is one factor that targets the promoters of different oncogenes or the genes that suppress tumor for the transcriptional repression or activation. The function of KLF8 in breast cancer was identified, when KLFB was identified as a kinase focal adhesion downstream effector.KLF8is known to be overexpressed in the human cancers that are invasive, such as breast cancer, hence promoting the invasion of the breast cancer cells togehte rwith metastasis. This happens through the propulsion through cycle cell progression. Due to the valid functions of KLF8, the protein is always regulated at the post transitional and transitional levels together with the localization of the nuclear. From the conducted studies, there is no documented study that reports on the molecular mechanism signalling by KLF8 and known to facilitate breast cancer. IN metastasis, and tumor invasion the matrix metalloproteinase has a vital function to play. They operate downstream of FAK by enhancing tumor metastatis. Another study on this field identified MMP9 as one direct transcriptional target of activation by KLF8 together with the mediator promoting KLF8 breast cancer invasion of cell. Togehter with that finding, the study established that KLF8 can regulate the MMP2 3nzyme functions with no effect to the expressional levels. Explanation. For the invasiveness of breast cancer ceel, the KLF8 upregulation of MMP14 is vital. A study by Lu et al (2013) showed that the KLF8 overexpression in the cells of MCF-10 would facilitate the knockdown and invasion of the KLF8 inside the MDA-MB-231 invasion cells. This study found that MMP9 is a transcriptional target of activation of the KLF8 in the cells which take part in the invasion of KLF8 invasion dependent (Symowicz & Adley, 2007). The activity of MMP2 is reported to be upregulated through KLF8 and the ewxpression message of the MMP2 enzyme activation. It was also established that MMP14 was upregulated by the KLF8 in the different cell lines, as determined by theanalysis of the microarray of the the KLF8 gene dependent profile expression. Lu et al (2013), attempted to verify the results using the reverse PCR transcriptase, and the real time PCR real-time quantitative. The out come was the KLF8 overexpression in the cells of 10A-iKB, there were the unpredicted expressional message of the MMP14 and the KLF8 knockdown in the 231-K8ikd cells. This is as a result of the MMP14 expressional message by not having any effect on theMMP2 expressional message. The obtained outcome shows out that the MMP14 are a KLF8 target transactivation and that the dependency of KLF8 increases in the MMP14 expression, hence other mechanism taking part in the cell invasion of KLF8. This study established a novel FAK and KLF8 to the MMP14 mechanism of signalling for the growth invasion and the lung metastasis in breast cancer. The model presents a high aberrant expression of KLF8 inside the cells of cancer,hence ensuring higher levels of MMP14. Additionally, the MMP14 transcription of genes is stimulated by the KLF8 through a direct binding on the promoter of the gene. In the nucleus, KLF8 is responsible for enriching the B-catenin through the representation of the E-cadherin expression together with increased translocation of B-catenin to the nucleus. The main effect is that the tCF1 would be regulated. Increased levels of TCF1 and B-catenin in the nuclear will lead to high activation of MMP14 trnscription gene. This occur whenever the interaction of TCF1 and B-catenin occurs. After the production of increased levels of MMP14 in the cells, active FAK is required to maintain the increased MMP14 protein ont he surface of the cell. In this case, the internalization MMP14 protein degradation would be prevented. Given these processes, there would be a guaranteed maximum role of MMP2 needed on the cell surface for the activation of the substrates such as MMP2 needed in the re-modeling of other metastasis, and tumor invasions. This information is shown in disgram 1. Diagram1. Following the basic function of the MMP14 in the growth of metastasis, and tumor, there are a number of processes, which ensures that a constant activation is maintained. This means that the fact that KLF8 enhances the activation of MMP14, it minimizes the regulation of MMP14 cell expression. This is similar to the function of KLF8 in regulating the other genes of target. Under the plasma membrane, the prevention the E-cadherin formation is one mechanism that can be useful in maintaining the existence of B-catenin in the nucleus. References Ara T, & Deyama Y. 2000. Membrane type 1-matrix metalloproteinase expression is regulated by E-cadherin through the suppression of mitogen-activated protein kinase cascade. Cancer Lett; 157: 115–121. Cristofanilli M. 2006. Circulating tumor cells, disease progression, and survival in metastatic Dwivedi, DJ, 2006. Matrixetalloproteinase inhibitors suppress transforming growth factor-Beta-induced subcapsular cataract formation. Am J Pathol; 168: 69–79. Lu, N, Wang, X, Wason, MS, Zhao, J, & Urvalek, AM. 2007. KLF8 and FAK cooperatively enrich the active MMP14 on the cell surface required for the metastatic progression of breast cancer breast cancer. Semin Oncol; 33(3 Suppl 9): S9–14. Nawrocki-Raby, B, & Gilles C. 2003. Pregulation of MMPs by soluble E-cadherin in human lung tumor cells. Int J Cancer 2003; 105: 790–795. Symowicz J, & Adley BP, 2007. Engagement of collagen-binding integrins promotes matrix metalloproteinase-9-dependent E-cadherin ectodomain shedding in ovarian carcinoma cells. Cancer Res; 67: 2030–2039. Veeman MT, & Slusarski DC. 2003. Zebrafish prickle, a modulator of noncanonical Wnt/Fz signaling, regulates gastrulation movements. Curr Biol; 13: 680–685. Zhao JH, & Reiske H. 1998. Guan JL. Regulation of the cell cycle by focal adhesion kinase. J Cell Biol; 143: 1997–2008. Read More