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Cancer Biology and Genetics for Non-Biologists
Published in Trevor F. Cox, Medical Statistics for Cancer Studies, 2022
Cell signalling is very complex. The sending of an initial signal to the final outcome induced by the signal usually involves many proteins and hence genes. The route taken to achieve the outcome is via a cell signalling pathway. For example, the MAPK/ERK pathway, also known as the Ras/Raf/MEK/ERK pathway, plays a significant role in cell growth and differentiation (the process where immature cells develop to reach their specialised form and function). The MAPK family is a set of mitogen-activated protein kinases (a kinase is a particular type of enzyme) produced by particular genes such as MAPK1, MAPK3, …MAPK15. These have other names, for example, MAPK1 is also known as ERK. A very simplified version of the MAPK/ERK pathway is,
Garcinia indica (Kokum) and Ilex aquifolium (European Holly)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Dicson Sheeja Malar, Mani Iyer Prasanth, Tewin Tencomnao, James Michael Brimson, Anchalee Prasansuklab
Network pharmacological approach suggests that UA acts against colon cancer cells by targeting 113 proteins including MAPK3, VEGFA, TNF, and STAT-3 indicating its multitargeted potential (Zhao et al., 2021). Further UA is also reported to target MMP9/CDH1, Akt/ERK, COX-2/PGE2, p300/NF-κB/CREB2 simultaneously to inhibit cell proliferation (Wang et al., 2013). Studies also report that UA inhibits the metastasis and invasiveness of colon cancer cells, which could be due to the attenuation of epithelial-mesenchymal transition, TGF-β1/Smad/FAK signaling pathways, and upregulation of miR-200a/b/c (Zheng et al., 2021; Prasad et al., 2012; Zhang et al., 2019b; Wang et al., 2019a).
Milroy Disease
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Expressed mainly in lymphatic endothelia, FLT4 interacts with VEGFC (which is a key regulator of blood vessel development in embryos and angiogenesis in adult tissues), enhances VEGFC production, promotes growth, survival, and migration of endothelial cells, and contributes to adult lymphangiogenesis and the buildup of the vascular network and the cardiovascular system during embryogenesis. In addition, FLT4 mediates activation of the MAPK1/ERK2, MAPK3/ERK1 signaling pathway, the MAPK8 and the JUN signaling pathway, and the AKT1 signaling pathway, and promotes phosphorylation of PIK3R1 (regulatory subunit of phosphatidylinositol 3-kinase) and MAPK8 at “Thr-183” and “Tyr-185”, and of AKT1 at “Ser-473” [8,9].
Deciphering metabonomics biomarkers-targets interactions for psoriasis vulgaris by network pharmacology
Published in Annals of Medicine, 2018
Jiangyong Gu, Li Li, Dongmei Wang, Wei Zhu, Ling Han, Ruizhi Zhao, Xiaojie Xu, Chuanjian Lu
And more notably, six proteins which were common proteins in all three systems played important roles in the three MBTNs. P01375 (Tumour necrosis factor alpha), P27361 (Mitogen-activated protein kinase 3), P29474 (Nitric oxide synthase [NOS], endothelial), P35228 ( NOS, inducible), P35354 (Prostaglandin G/H synthase 2), P42345 (Serine/threonine-protein kinase mTOR) were extensively involved in inflammation, immune response and cell proliferation. Tumour necrosis factor-alpha (TNF-alpha) can stimulate cell proliferation and induce cell differentiation [44]. Mitogen-activated protein kinase 3 (MAPK3) is an essential component of the MAP kinase signal transduction pathway and mediates diverse biological functions, such as cell growth, adhesion, survival and differentiation (from the UniProt database [18]). Serine/threonine-protein kinase mTOR (TOR) is a central regulator of cellular metabolism, growth and survival [45,46]. NOS and Prostaglandin G/H synthase 2 (COX2) can produce nitric oxide (NO) and prostaglandin H2 (PGH2). PGH2 can be converted to PGE2 by Prostaglandin E synthase. In our previous study, NO and PGE2 were both important inflammatory biomarkers [23,24]. Therefore, the six proteins could be important targets for psoriasis.
Role of granulosa cell mitogen-activated protein kinase 3/1 in gonadotropin-mediated meiotic resumption from diplotene arrest of mammalian oocytes
Published in Growth Factors, 2018
Kankshi Sahu, Anumegha Gupta, Alka Sharma, Meenakshi Tiwari, Ashutosh N. Pandey, Shilpa Prasad, Pramod K. Yadav, Ajai K. Pandey, Tulsidas G. Shrivastav, Shail K. Chaube
Mitogen-activated protein kinases 3/1 (MAPK3/1) is serine/threonine (Ser/Thr) kinases and commonly expressed in wide variety of eukaryotic cells (Kyriakis & Avruch, 2012; Peti & Page, 2013). It regulates important cellular processes including gene expression, cell proliferation, differentiation, metabolism and apoptosis (Arthur & Ley, 2013; Kalous et al., 2018; Liu et al., 2007). Three isoforms of MAPK3/1 are most extensively studied in mammalian cells. These includes p38 MAPK α, β, γ, and δ isoforms; the c-JUN N-terminal kinase 1, 2, 3 (JNKs) and the ERK1/2 (Chen & Cobb, 2001; Owens & Keyse, 2007; Pearson et al., 2001). These isoforms are induced by ultraviolet radiation, oxidative stress and by cytokines (Pimienta & Pascual, 2007). Activated MAPK3/1 move from cytosol to the nucleus where they phosphorylate the Ser/Thr residues of many substrates implicated in stress responses, growth inhibition and apoptosis (Kalous et al., 2018; Owens & Keyse, 2007).
MiRNA-375 inhibits retinoblastoma progression through targeting ERBB2 and inhibiting MAPK1/MAPK3 signalling pathway
Published in Cutaneous and Ocular Toxicology, 2022
Lei Liu, Chunlin Xiao, Qiuyun Sun
Previous studies have shown that MAPK1/MAPK3 pathway was involved in various tumours development, and EMT is associated with tumour invasion and metastasis28. A number of molecules, such as E-cadherin, N-cadherin, and Vimentin are considered to be key markers of EMT 29. Here, the effect of miR-375 on EMT and MAPK1/MAPK3 pathway was investigated in RB cells. As Figure 5(A) shown, over-expression of miR-375 enhanced the level of E-cadherin, while inhibited the levels of N-cadherin and Vimentin in Y79 and SO-RB50 cells. Furthermore, up-regulation of miR-375 repressed the related protein of MAPK1/MAPK3 pathway, including p-MAPK1/3, VEGF, and MMP-2 (Figure 5(B)). These results indicate that miR-375 inhibit EMT and MAPK1/MAPK3 pathway in RB cells.