The Expression Of Matriptase Centered On Lung Cancer Cells

HeLa cells are the most widely used human cell lines in existence. They are used in many experiments. For example, recent studies have shown that expression of girdin is associated with types of cancer. The expression of gidin was suppressed when in HeLa cells in vitro which allowed the gidin to be evaluated. It was found that patients with high-grade cervical cancer tumors exhibited strong expression of girdin. It appeared that girdin is key in HeLa cell

Aim 2: To identify the proteins in the exosome of the metastatic cancer cells. The exosome or the secretory vesicle fraction will be concentrated from the extracellular media of metastatic, non-metastatic cancer cell and compare with the control cells. SILAC labelled proteomic analysis will be performed in the isolated exosomes to identify the proteins that are specific in metastatic cells.

Cancer is listed as the second most common cause of death in western countries; particularly, in adults. Though it has a long antiquity, its prevalence and incidence today is pervasive and the war on cancer has not been promising. Malignant neoplasia is characterized by uncontrolled growth and the ability to metastasize or spread from the original site. Cancer results from mutations that promote cell proliferation and inhibit cell adhesion (metastasis). According to the National Cancer Institute (2016), “Cancer can also spread regionally,

Hyaluronan (HA) is an extracellular matrix component that is secreted by fibroblasts and also works in inhibiting cell division. In a research article by Dr. Tian et al., They propose a mechanism for the cancer resistance exhibited by naked mole rats. They observed that in naked mole rats, there are greater levels of high molecular weight HA excreted from their fibroblasts. This high molecular weight HA accumulates in the tissues of the naked mole rat because the enzyme that is responsible for degrading, hyaluronan synthase 2, has decreased activity. When experiments are performed to remove HA, by the two methods, knocking down HAS2 or causing the overexpression of the enzyme Hyal2 which is responsible for the degradation of HA, the cells of

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

Cancer is an abnormal growing cells in which regulation of normal cell division is altered causing normal cells to acquire abnormal functions resulting from a series of molecular events that altered the normal properties of the cells(Schneider, 2001). The resultant aberrant cell behavior leads to the massive spread of abnormal cells that destroy surrounding normal tissue and invade other vital tissues(Alison, 2001). These uncontrolled, abnormal cells no longer

Importantly, the ERM protein ezrin itself is a well-known mediator of metastasis (Elliott et al., 2005; Khanna et al., 2004; Meng et al., 2010). Many clinical studies have linked high expression of ezrin with poor outcome in cancer patients suffering from a wide variety of cancers, including prostate, breast can lung cancer (Clucas and Valderrama, 2014). Interestingly, specifically the abnormal distribution of ezrin in breast cancer patients, from the apical regions of non-tumorigenic cells to motile projections in invasive cells, has been correlated with poor prognosis (Sarrio et al., 2006). In addition, it has previously been indicated as an important regulator of metastasis in the murine carcinoma cell line AC2M2 (Elliott et al., 2005). Furthermore, ezrin overexpression has been shown in various studies to promote the survival, migration and/or invasion of cancer cells into surrounding tissue and to disrupt cell-cell contacts (Clucas and Valderrama, 2014).

This demonstrates the urgency and need to study these family of proteins in effort to treat

Many gene targets have been used in the antineoplastic therapy. Up to now, mainly chemical inhibitors have been used to inhibit growth of cancer cells. Chemical inhibitors, however, have the intrinsic disadvantage that they often evoke nonspecific side effects (19). The current antisense technologies provide an attractive alternative but usually can only inhibit the expression of gene transiently and partially. The key features of glioma are growth and opposing cell apoptosis. Interactions with the extracellular matrix (ECM) are likely to play an important role in regulation of glioma cell growth (20). Cyr61, a cysteine-rich, heparinbinding, protein that is secreted and associated with the cell surface and ECM (21). It has been proposed that Cyr61 proteins function primarily as matricellular proteins and bridge the functional separation between structural macromolecules in the ECM and effector molecules such as growth factors and cytokines (22). Given the central role of the ECM in cell homeostasis (23), Cyr61 proteins are able to influence cell function by their regulation of ECM production as well as by binding to specific ECM components. Therefore, we tried to determine the roles of Cyr61 by acting on integrin- ECM in the human glioma.

Local invasion represents the first step of the metastatic cascade and requires profound changes in cell-cell adhesion, cell-ECM interactions, proteolysis of ECM components and acquisition of migratory properties. Cancer cells can deploy different types of cell migration, including collective migration and single cell migration50. Predominantly, most epithelial cancer cells use collective cell migration, however some cancer cells may co-opt the biological program known as the EMT to migrate as single cells. EMT is a critical process for multiple aspects of normal embryonic development51. Since its discovery, there has been the realization that there are many parallels in the mechanisms that govern EMT in embryonic development and in cancer

CN’s dimeric structure results in high reactivity in platelet protein phosphorylation, allowing CN to bind to IIb3 and inhibiting platelet aggregation. It is also known that CN is able to bind to 1 and 3 subclasses, inhibiting many types of integrins (Lin et al. 2010). Research has shown that the two integrins that are expressed in angiogenesis and cancer metastasis are v3 and v5. Blocking v5 results in blocking the vascular endothelial growth factor, or VEGF, angiogenesis because of its involvement in cell adhesion. This integrin requires an insulin growth factor to activate to mediate cell migration. Zhou et al. (2000) has shown that CN binding to vitronectin receptors allows the inhibition of melanoma and breast cancer cells to vitronectin. In addition, v3 commonly mediates tumor cell adhesion to vitronectin. However, antagonists to this integrin can inhibit angiogenesis in endothelial cells, with CN acting as an antagonist. Many studies have tested the efficacy of CN on tumors from breast cancer, prostate cancer, and bladder cancer. For example, CN was able to inhibit the adhesion of T24 bladder carcinoma cells to vitronectin (Zhou et

A study done by Jian et al looked at what role the KAL1 gene plays played in other physiological and pathological processes besides migration of GnRH neurons in embryogenesis. The study investigators screened colon, lung, and ovarian cancer for KAL1 gene expression. They observed a decrease in KAL1 expression was decreased in these tissues compared to uninvolved tissues. However, as the cancer progressed to stage II and then on to stage III and IV the expression of KAL1 increased at each stage. The study then found a direct correlation between KAL expression and TGFβ in colon cancer. The study also found that TGFβ induces KAL1 gene expression and secretion of the Anosmin-1 protein. Anosmin-1 protected cancer cells from apoptosis activated

Breast cancer development involves a specialized cell surface protein which is thought to regulate growth of tumor cells. Dr. Marcia L. Graves et at. investigated the effects of this protein in breast cancer cells and found that it promotes development and movement of breast cancer cells.

Specific aims: EGFR and c-Met are receptor tyrosine kinases (RTKs), and tyrosine kinase inhibitors (TKIs) against these receptors have been initially effective when prescribed to patients in combination with traditional chemotherapy or radiation. However, the overall efficacy of TKIs is limited due to the development of resistance as seen through clinical trials in NSCLC. Epithelial Mesenchymal Transition (EMT) is a process by which epithelial cells undergo phenotypic and morphological changes to acquire mesenchymal characteristics including increased motility and invasiveness. Currently, the role of EMT in TKI drug resistance is poorly understood. EMT results in loss of tight junction proteins such as E-cadherin and upregulation of transcriptional repressors of these proteins such as ZEB1. Recently, protein arginine methyl transferase 1 (PRMT1) has been shown to be an important regulator of EMT, cancer cell migration and metastasis. However, the role of PRMT1 in TKI resistance is not known. In this study, we propose to evaluate the role of EMT proteins in TKI resistance using H2170 and H358 cell lines (wild type EGFR) that were made resistant to an EGFR inhibitor, erlotinib and a c-Met inhibitor, SU11274 and a combination of both. H3255 cell line (with L858R EGFR mutation), and H1975 cell line with L858R and T790M EGFR mutations which we have made resistant to erlotinib will also be used. Our recent in vitro studies indicate that TKI resistance may be due to the activation

In cancer settings, Chen et al. demonstrated that CEP55 overexpression is associated with hepatocellular carcinoma (HCC) and lung adenocarcinoma and results in promoting invasion and cell migration via upregulation of the PI3K/AKT pathway [247, 248]. As discussed previously, VEGF-A persuades CEP55 expression and hence PI3K/AKT pathway in a dose dependent manner in lung cancer cell lines. Notably, VEGF-A stimulate translocation of CEP55 to the plasma membrane from cytoplasm [248]. In addition, VEGF-A is a compelling stimulator of endothelial cell vascular permeability, motility, proliferation and angiogenesis with well-established role in cancer [250]. Consistently,