Abstract:
:Recent global incidences and mortality rates have placed colorectal cancer (CRC) at third and second positions, respectively, among both sexes of all ages. Resistance during chemotherapy is a big problem in the treatment and disease-free survival of CRC patients. Discovery of new anticancer drug(s) is a time taking process and therefore, invites studies for repurposing the known therapeutics. The present study was conceived to analyze the anticancer role of Imatinib in experimental CRC at early stages. Different experimental procedures e.g. tumor incidences or histoarchitectural changes, gene and protein expression analysis, estimations of intracellular calcium, ROS, mitochondrial membrane potential, apoptotic index and molecular docking was performed to support the hypothesis. It was observed that Imatinib could function as an immunomodulator by breaking the feed-back loop between the proinflammatory cytokines (IL-1β and TNF-α) and transcription factors (NF-κB, Jak3/Stat3) knowingly involved in increased cell proliferation during tumorigenesis via activating different intracellular signaling. Also, Imatinib could independently deregulate the other cell survival and proliferation signaling e.g. PI3-K/Akt/mTOR, Wnt/β-catenin and MAPK. Proinflammatory cytokines orchestrated intracellular signaling also involve angiogenic factors to be upregulated during CRC which were also seemed to be independently suppressed by Imatinib. Restoration of physiological apoptosis by increasing the release of intracellular calcium to generate ROS thereby reducing the mitochondrial membrane potential for the release of cytochrome c and activation of caspase-3 was also reported with Imatinib administration. Thus, it may be suggested that Imatinib show synergistic pleiotropy in suppressing the interlinked tumorigenic signaling pathways independently.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Dhiman DK,Sanyal SN,Vaish Vdoi
10.1016/j.cellsig.2020.109803subject
Has Abstractpub_date
2020-12-01 00:00:00pages
109803eissn
0898-6568issn
1873-3913pii
S0898-6568(20)30280-1journal_volume
76pub_type
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abstract::Certain TRP cation channels confer the ability to sense environmental stimuli (heat, cold, pressure, osmolarity) across physiological and pathophysiological ranges. TRPA1 is a TRP-related channel that responds to cold temperatures, and pungent compounds that include the cold-mimetic icilin and cannabinoids. The initia...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2005.12.009
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abstract::The type II epithelial-mesenchymal transition (EMT) produces airway fibrosis and remodeling, contributing to the severity of asthma and chronic obstructive pulmonary disease. While numerous studies have been done on the mechanisms of the transition itself, few studies have investigated the system effects of EMT on sig...
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pub_type: 杂志文章
doi:10.1016/j.cellsig.2015.03.024
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abstract::Both type I interferons (IFNs) and interferon regulatory factors (IRFs) are well characterized in viral infections, whereas they are far less studied in bacterially activated toll-like receptor (TLR) pathways. Here, we studied the involvement of IRF1 and IRF2 in TLR2-mediated responses. In mouse macrophages, IRF2 was ...
journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2008.06.017
更新日期:2008-10-01 00:00:00
abstract::Lithium is an anti-depressant drug that also possesses immunomodulatory functions. The anti-inflammatory effect of lithium is thought to involve activation of the transcription factor CREB, although the underlying mechanism is incompletely understood. We show here that in macrophages lithium stimulates Tpl2, a MAP kin...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2008.12.010
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pub_type: 杂志文章
doi:10.1016/j.cellsig.2018.10.021
更新日期:2019-01-01 00:00:00
abstract::Plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of urokinase-and tissue-type plasminogen activators (uPA and tPA), is an injury-response gene implicated in the development of tissue fibrosis and cardiovascular disease. PAI-1 mRNA and protein levels were elevated in the balloon catheter-injured carotid...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2015.01.009
更新日期:2015-05-01 00:00:00
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journal_title:Cellular signalling
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
doi:10.1016/j.cellsig.2011.07.013
更新日期:2011-12-01 00:00:00
abstract::NO-sensitive guanylyl cyclase (GC) acts as the effector molecule for NO and therefore plays a key role in the NO/cGMP signalling cascade. Besides the long known GC isoform (alpha(1)beta(1)), another heterodimer (alpha(2)beta(1)) has recently been identified to be associated with PSD-95 in brain.Here, we report on the ...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/s0898-6568(02)00078-5
更新日期:2003-02-01 00:00:00
abstract::The orthologous proteins of the stress-activated protein kinase-interacting 1 (Sin1) family have been implicated in several different signal transduction pathways. In this study, we have investigated the function of the full-length human Sin1 protein and a C-terminally truncated isoform, Sin1alpha, which is produced b...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2004.10.015
更新日期:2005-06-01 00:00:00
abstract::Extracellular adenine dinucleotides are modulators of blood vessel tone. We have previously demonstrated that Ap(2)A and Ap(4)A induce the synthesis of nitric oxide (NO) from bovine aortic endothelial cells (BAEC) while Ap(3)A and Ap(5)A do not [FEBS Lett. 427 (1998) 320; Arch. Biochem. Biophys. 364 (1999) 280.]. In t...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/s0898-6568(00)00147-9
更新日期:2001-02-01 00:00:00
abstract::Alzheimer's disease (AD) is a neurodegenerative illness and the leading cause of dementia in the elderly. The accumulation of amyloid-β peptide (Aβ) is a well-known pathological hallmark associated with the disease. However, Aβ is only one of several metabolites produced by β- and γ-secretase actions on the transmembr...
journal_title:Cellular signalling
pub_type: 杂志文章,评审
doi:10.1016/j.cellsig.2011.10.007
更新日期:2012-02-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/0898-6568(95)02051-9
更新日期:1996-03-01 00:00:00
abstract::Signal transducer and activator of transcription 1 (STAT1) is an important mediator for cytokine signal transduction, particularly IFN-γ. Following IFN-γ stimulation, STAT1 is activated through tyrosine phosphorylation. Little is known about the function and regulation of STAT1 dephosphorylation after activation. We s...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2011.04.003
更新日期:2011-08-01 00:00:00
abstract::In humans, thromboxane (TX) A₂ signals through the TPα and TPβ isoforms of its G-protein coupled TXA₂ receptor (TP) to mediate a host of (patho)physiologic responses. Herein, angio-associated migratory cell protein (AAMP) was identified as a novel interacting partner of both TPα and TPβ through an interaction dependen...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2010.12.003
更新日期:2011-04-01 00:00:00
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pub_type: 杂志文章,评审
doi:10.1016/j.cellsig.2008.07.011
更新日期:2009-01-01 00:00:00
abstract::The striking clinical benefit of PTH in osteoporosis began a new era of skeletal anabolic agents. Several studies have been performed, new studies are emerging out and yet controversies remain on PTH anabolic action in bone. This review focuses on the molecular aspects of PTH and PTHrP signaling in light of old player...
journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2009.02.012
更新日期:2009-08-01 00:00:00
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journal_title:Cellular signalling
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2014.04.003
更新日期:2014-08-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2009.08.003
更新日期:2009-12-01 00:00:00
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2008.04.010
更新日期:2008-08-01 00:00:00
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更新日期:2019-08-01 00:00:00
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doi:10.1016/j.cellsig.2018.11.024
更新日期:2019-02-01 00:00:00
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更新日期:2014-04-01 00:00:00
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journal_title:Cellular signalling
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2011.12.001
更新日期:2012-04-01 00:00:00
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