Olivia Matheu
Bio 206
Assignment #3
Detailed focus question: Cell migration is the movement of cells in a specific direction in order to perform a specific task. Cell migration is necessary in maintaining a healthy organism. In spite of this what type of outside factors prevent, slow down, increase, or enhance cell migration and why? How does this affect the organism overall?
Introduction: Provide background information on cell migration and its importance. Then I will discuss the different factors that have an effect on cell migration. I will focus on the different influences that prevent successful cell migration. The three main points are cancer cells, MIIP, a cytoskeleton regulator, and development of tumors
Main Discussion Points:
A. Cancer
1. Cells migrate faster
2. EMT- epithelial cells lose their polarity
3. Different types of migration (microtubules)
B. MIIP- Cytoskeleton regulator
1. Blocks cell migration and invasion
2. Delays mitosis
3. Suppresses tumorigenesis
C. Tumors
1. P53
2. Tumor suppressor
3. Can develop to drive or prevent cell migration
II. This section will focus on the influence cancer has on the development, growth, and migration of individual cells.
A. A cancer cell: cells that continually grow and develop.
B. An Epithelial-mesenchymal transition (EMT) plays a role in the development of cancer cells.
1. EMTs is when the adhesion protein E-cadherin is suppressed.
2. Metastasis and stem-like growth in cancer cells is promoted. Treatment resistance.
Breast Cancer is a type of cancer where in the breast cells growth are uncontrolled. To enhance our understanding of breast cancer, knowing how any cancer can develop is crucial. Cancer develops as a result of the alteration of the genes, or abnormal changes in the genes accountable for managing the growth of the cells and maintaining their health. In each nucleus, the genes operates as the “control room.” The cells in our bodies replace themselves through a process called cell growth in which the
Various speculations of how cancer is produced have been looked into through numerous years and
Cancer is often conceived as a single disease. The general idea of cancer deals with the proliferation of cell division amounting into tumors. The cause of cancer and how it’s treated is what scientists have spent decades trying to understand. In recent decades, scientists have been effective in characterizing the “hallmarks” of cancer and better understanding the disease through the use of molecular biology techniques. Additionally, scientists have been successful in understanding the influence that environmental factors and genetics play in the progression of cancer. Cancer is now understood to be caused by the mutation of genes leading to the activation/inactivation
Cancers seem to develop progressively. There will be intermediate stages between those normal cells and highly altered cells. Hyperplasia is the first stage in which cells look normal but with increased cell number. Next stage is dysplasia, characterized by more cytologically abnormal cells. Dysplasia is followed by metastasis stage, where cells can invade new tissues. During transformation from normal cells to altered cells, either inhibition of tumor suppressor gene or activation of anti-apoptotic genes happen. Almost in all cancers, cell cycles regulators are mutated. Main hallmarks of cancer include induction of angiogenesis, activation of the oncogene, suppression of apoptotic or tumor suppressor gene, activation
Cancer occurs when cells in a part of the body, such as the colon grow
The factors limiting the growth of malignant neoplasm include the basal membrane and various components of the surrounding stroma, increased interstitial pressure, limited oxygen supply to tumor cells and the formation of active oxygen forms, hypoxia conditions, and permanent exposure to immune system cells. Given the intra-tumoral heterogeneity, in the struggle for survival, some tumor cells may be subjected to regression and death, while other cells, which resist powerful, counteracting micro-environmental factors, gain an aggressive phenotype and the ability of metastatic progression. Invasive tumor growth is enabled by the detachment of malignant cells from the tumor mass due to a reduction in or complete loss of intercellular adhesion molecules, and, therefore, the cells gain the ability of anomalously high motility enabling penetration through the stiff structural elements of the surrouss means the ability to thrust aside adjacent tissues, and also to actively invade and, therefore, destroy these
In the one hand, IL-6 inhibited cell proliferation by independent pathways involving STAT3 activity. On the other hand, IL-6 stimulated cell migration by activating MAPK/PI3K pathway(15). Interestingly, hypoxia potently induced IL-6 expression and signaling(16). Recently, hypoxia has been shown to promote metastatic features such as migration, invasion, and EMT characteristics(17). 这几句与前面的联系是什么?为何突然引出?Several studies have addressed the role of IL-6 in tumor cell growth and migration in vitro, but its exact role remains varied and unclear. Yet a mechanistic link between IL-6 and progressive disease in breast cancer patients remains poorly
Overall, the world has witnessed a significant increase in the number of people suffering from different types of cancer (Agarwal,2011). These types have many causing agents and have been divided into physical carcinogens, chemical carcinogens and biological carcinogens (ibid). However, according to Agarwal, one of the most common causes is related to lifestyle. Regardless of the different causes, however, the effect will be thee same. Cancer impairs the body as a consequence of uncontrolled cells division and tissue swells to form tumors (Agarwal,2011).
It is the consensus that cancer is a form of disease that portrays itself in various ways. Cancer is the abnormal multiplication of the cell. Interestingly, Hosick, Rizzo, Campanella and Alder (2017) have argued that cancer is inappropriate and uncontrollable cell growth within one of the specialized tissues of the body, threatening normal cell and organ function and in serious cases travelling via the bloodstream to other areas of the body. This irregular cell growth can start anywhere in the body for example; in the blood, lungs, breast or the pancreas.
Association of cancer cells with TAMs throughout the tumour significantly increases their motility, this gets further amplified when cancer cells are found in close proximity to perivascular TAMs. Moreover, cancer cells were observed to invade blood vessels only where perivascular TAMs were located.
The afore mentioned intricate network of interactions during EMT leads to many important changes in the phenotype and behavior of the cells. Epithelial cells undergo prominent morphological changes including the loss of cell-cell adhesion and the loss of apical-basal polarity. The cobblestone-like monolayer of epithelial cells with an apical-basal polarity is converted to dispersed, spindle-shaped mesenchymal cells with migratory protrusions. In addition to these morphological changes, cells undergoing EMT loose the expression of E-cadherin and other epithelial differentiation markers and gain the expression of mesenchymal markers such as vimentin, N-cadherin and fibronectin. These changes lead to the acquisition of migratory and invasive properties which enable the cells to migrate and invade through the ECM and the adjacent stroma (Boyer and Thiery, 1993). Thus, during cancer progression the EMT confers all the traits to the carcinoma cells which are required to overcome natural tissue barriers on their way to metastasis formation. These gained traits go hand in hand with a reduced proliferative potential of the mesenchymal-like tumor cells (Vega et al., 2004).
With the help of chemokines, cytokines and growth factors secreted by tumor cells, macrophage are recruited to the site of tumors. These macrophages and tumor cells will then secrete IL-1 which will allow angiogenesis, matrix remodeling, metastasis and invasion to occur, resulting in tumor progression. [1]
Though the previous experiment does indicate that when a seed is inserted into a cell it can form amyloid fibers, it fails to include parameters that describe how these proteins are transferred between cells. In order for an infectious agent to become infectious it must have a method for not only leaving the host cell but also entering a non-infected cell. A study lead by Christian Münch set out to show the pathway that a prion like protein in an amyloid fiber can transfer between cells. The first test that was done in this study was to grow cells in a media containing a mutant SOD1 (a common ALS causing protein) granule coated fibrils. These fibrils were labeled with Dylight dyes and when examined the majority of the grown cells were
According to the stochastic model, tumor cells are biologically equivalent but their behavior is influenced by intrinsic and extrinsic factors and is therefore both variable and unpredictable. Thus, tumor-initiating activity cannot be enriched by sorting cells based on intrinsic characteristics.
4) Metastasis: metastases are tumour implants discontinuous with the primary tumour. All cancers can metastasize except those of glial cells in CNS (Gliomas), and basal cell carcinoma of the skin but they are locally invasive. Pathways of spread: i) Seeding of body cavities and surfaces: esp. carcinoma of ovaries and sometimes mucus-secreting appendiceal carcinoma fill the peritoneal cavity with a gelatinous neoplastic mass referred to as pseudomyxoma peritonei. ii) Lymphatic spread: is the most common pathway for the initial dissemination of carcinomas, and sarcomas as well. The pattern of lymph node involvement follows the routes of lymphatic drainage. A Sentinel Lymph Node is defined as the first node in a regional lymphatic basin that receives