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  • TRIM expression was associated with serum

    2019-04-22

    TRIM7 expression was associated with serum HBV DNA copy number of HCC patients. HBV infection is the main risk factor for HCC [2]. Increasing evidence has supported the oncogenic role of HBx, a protein coded by HBV, in HCC. HBx is able to regulate cell proliferation, naag progression and cytokine production by interfering with various signaling pathways such as the WNT/β-catenin, PI3K/AKT and MAPK pathways [28]. In the current study, TRIM7 expression was enhanced in the presence of HBx. HBx had the same effects as TRIM7 overexpression on the expression of DUSP6, p-p38, p53 and p21, which was suppressed by TRIM7 knockdown. Overall, these results inferred that TRIM7 expression was regulated by HBx. Further experiments are needed to explore the detailed regulatory mechanism.
    Acknowledgements These studies were supported by grants from cooperation (Shanghai Shenkang Medicine Developing Project) of China [grants number: SHDC12017104] and the National Natural Science Foundation of China (grants No. 81770589 and No. 81470853).
    Introduction Lung cancer remains at the top of the list of the world\'s deadliest cancers and is the second greatest cause of morbidity and mortality worldwide (Jemal et al., 2011). Despite, advances in early detection and standard treatment, non small cell lung cancer is often diagnosed at an advanced stage and has a poor prognosis. Although smoking remains the primary cause of most lung cancers, the mechanism by which cigarette smoke spurs cancer development are not fully understood. The treatment and prevention of lung cancer are major unmet needs that can probably be improved by a better understanding of the molecular origins and evolution of the disease. MAPKinase pathway participates in various intracellular signaling pathways that control at all round of cellular processes that include growth, differentiation and stress responses which have a key role in cancer progression. The study of signaling molecule expression, functional and therapeutic response during the cancer progression and treatment are becoming important day by day. p38MAP kinases contains four isoforms, i.e., p38α, p38β, p38γ, and p38δ, their roles in several cancers identified based on expression patterns, substrate specificities and sensitivity to chemical inhibitors. p38MAPK can be further divided into two groups (Wong, Todd, Tsuji, and Donoff, 1996). One group includes p38α and p38β, which are homologus and have overlapping functions. In contrast p38γ and p38δ have restricted expression patterns and probably have specialized functions (Cobb, 1999). In earlier studies, researchers explained that human serum proteins originate from different tissues and enter the circulation as a result of secretion and leakage (Taylor, 1969). The study of serum protein marker is an important area of research. In case of the lung cancer, exact mechanism and expression pattern of all isoforms of p38MAPK still not known. The present study attempted to evaluate expression level of all four isoforms of p38 MAPK kinase signaling molecules in serum of NSCLC disease for the development of specific protein biomarker and accounting their therapeutic importance.
    Materials and method
    Results
    Discussion The importance of the p38 MAPK signaling pathway involved in cancer has been increasingly accepted (Liu, He, and Yang, 2015; Gonzalez-Villasana et al., 2015). Its diverse role is still contradictory, in cancers (Cuenda and Rousseau, 2007; Rennefahrt, Janakiraman, Ollinger, and Troppmair, 2005; Loesch and Chen, 2008). p38 MAPK has been reported to induce apoptosis in some cells, but prevent apoptosis in others (Chen et al., 2009). Conversely, a number of studies implicated p38 MAPK play a negative regulator for cell proliferation (Grossi, Peserico, Tezil, and Simone, 2014; Tai, Su, Chen, Jou, and Lin, 2014). p38 α is abundant in most cell types and is the best-described isoform in the literature and reported to be over-expressed in many cancers like oral (Riebe, Pries, Kemkers, and Wollenberg, 2007) breast (Davidson et al., 2006), gastric (Liang et al., 2005) and non small lung cancer (Greenberg et al., 2002).