ASK family in cardiovascular biology and medicine

Liu, Tingting; Zhou, Huanjiao Jenny; Wang, Min

doi:10.1016/j.jbior.2017.10.011

Cited by 12 publications

(10 citation statements)

References 93 publications

(109 reference statements)

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“…As KRAS has been frequently observed to be mutated in pancreatic cancer, attempts have been developed to generate effective RAS inhibitors as well as additional signaling molecules in this pathway. Attempts to inhibit the RAS/PI3K/PTEN/Akt/mTORC1/GSK-3 and other signaling pathways have been a central focus in many basic science laboratories and pharmaceutical companies for over three decades due to the involvement oncogenes in this pathway in human cancers (Yang et al, 2013;Fitzgerald et al, 2015;McCubrey et al, 2015;Anderson et al, 2016;Banfic et al, 2016;Cocco et al, 2016;Erneux et al, 2016;Falasca and Ferro, 2016;Fields et al, 2016;Geck and Toker, 2016;Maczis et al, 2016;Perdios et al, 2016;Pyne et al, 2016;Scarlata et al, 2016;Scoumanne et al, 2016;Tanaka et al, 2016;Ando et al, 2017;Carman and Han, 2017;Fujisawa, 2017;Geffken and Spiegel, 2017;Guo et al, 2017;Jang et al, 2017;Leonard and Johnson, 2017;Liu et al, 2017;Matsuzawa, 2017;McCubrey et al, 2017aMcCubrey et al, , 2017bMcCubrey et al, , 2017cMcCubrey et al, , 2017dObsil and Obsilova, 2017;Okazaki, 2017;Pyne et al, 2017;Ramos et al, 2017;Ratti et al, 2017;Rebello et al, 2017;Roth and Frohman, 2017;Rusnak and Fu, 2017;…”

Section: Introductionmentioning

confidence: 99%

Metformin influences drug sensitivity in pancreatic cancer cells

Candido

Abrams

Steelman

et al. 2018

Advances in Biological Regulation

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Pancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic malignancy and accounts for 85% of pancreatic cancers. PDAC patients have poor prognosis with a five-year survival of only 5-10% after diagnosis and treatment. Pancreatic cancer has been associated with type II diabetes as the frequency of recently diagnosed diabetics that develop pancreatic cancer within a 10-year period of initial diagnosis of diabetes in increased in comparison to non-diabetic patients. Metformin is a very frequently prescribed drug used to treat type II diabetes. Metformin acts in part by stimulating AMP-kinase (AMPK) and results in the suppression of mTORC1 activity and the induction of autophagy. In the following studies, we have examined the effects of metformin in the presence of various chemotherapeutic drugs, signal transduction inhibitors and natural products on the growth of three different PDAC lines. Metformin, by itself, was not effective at suppressing growth of the pancreatic cancer cell lines at concentration less than 1000 nM, however, in certain PDAC lines, a suboptimal dose of metformin (250 nM) potentiated the effects of various chemotherapeutic drugs used to treat pancreatic cancer (e.g., gemcitabine, cisplatin, 5-fluorouracil) and other cancer types (e.g., doxorubicin, docetaxel). Furthermore, metformin could increase anti-proliferative effects of mTORC1 and PI3K/mTOR inhibitors as well as natural products such as berberine and the anti-malarial drug chloroquine in certain PDAC lines. Thus, metformin can enhance the effects of certain drugs and signal transduction inhibitors which are used to treat pancreatic and various other cancers.

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Section: Introductionmentioning

confidence: 99%

Metformin influences drug sensitivity in pancreatic cancer cells

Candido

Abrams

Steelman

et al. 2018

Advances in Biological Regulation

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“…In the last two decades, the apoptosis signal-regulating kinase (ASK) family members ASK1, ASK2 and ASK3, the key molecules in MAPK signal cascade, have attracted much attention. ASK1 participates in the regulation of cell survival, proliferation, inflammation, and apoptosis [87]. Evidence has shown that ASK1 in response to OS and the bacterial component lipopolysaccharide (LPS) activates c-Jun N-terminal kinase (JNK) and p38 kinase which are involved in apoptosis and inflammation in response to stressful stimuli, where ROS are the stress mediators and control many cellular processes [87, 88].…”

Section: Discussionmentioning

confidence: 99%

“…ASK1 participates in the regulation of cell survival, proliferation, inflammation, and apoptosis [87]. Evidence has shown that ASK1 in response to OS and the bacterial component lipopolysaccharide (LPS) activates c-Jun N-terminal kinase (JNK) and p38 kinase which are involved in apoptosis and inflammation in response to stressful stimuli, where ROS are the stress mediators and control many cellular processes [87, 88]. The finding of Matsuzawa showed that the ASK1-p38 signaling pathway is critical for the formation of inflammatory cytokines (TNF- α , IL-6, IL-12, and IL-1 β ); these finding demonstrate ASK1 signaling is involved in mammalian innate immunity [88].…”

Section: Discussionmentioning

confidence: 99%

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Psychological Stress and Cellular Aging in Cancer: A Meta-Analysis

Kruk

Aboul‐Enein

Bernstein

et al. 2019

Oxidative Medicine and Cellular Longevity

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Background Epidemiological evidence continues to accumulate on the effect of psychosocial and behavioral factors in relation to cancer risk, progression, and mortality. Material and Methods This article presents the current evidence on the relationship between psychological stress and the risk of cancer and cellular aging process. Ten databases were searched to identify publications up to September 2019. References from retrieved articles were also reviewed. We included nine review papers and 26 cohort or case-control studies based on inclusion/exclusion criteria. Results Results of previously published review articles did not show consistent evidence for the association between cancer risk and psychological stress, while previous evidence is stronger regarding the role of chronic psychological stress on cancer growth and metastasis and aging. In seven observational studies, severe life events, anxiety, depression, insufficient social support perception, or avoiding coping strategy were significantly associated with breast cancer risk. For other specific types of cancer, 11 studies reported increased risk factors for stressful life events, and two others found increased mortality or a decline in treatment adherence. Conclusions Recent epidemiological evidence generally suggests psychosocial factors may be considered risk factors for specific types of cancer and play a key role in the cellular aging process. Understanding molecular mechanisms of the stress interaction is important in cancer management and prevention. The psychological stressors should be considered when developing or evaluating change in psychosocial practice.

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“…AIP1 plays an important role in several signaling pathways which are key regulators of chemokines known to be involved in transplant vasculopathy (Mitchell et al, 2007;Belperio and Ardehali, 2008). AIP1 inhibits the target molecules in a receptor-complex dependent manner (Luo et al, 2008;Huang et al, 2013;Ji et al, 2014;Ji et al, 2015;Liu et al, 2017;Yin et al, 2017;Zhang et al, 2018). We previously demonstrated that AIP1 binds to VEGFR2 and PI3K and forms a vascular endothelial growth factor-PI3K (VEGFR2-PI3K) complex (Luo et al, 2006;Zhang et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

AIP1 Suppresses Transplant Arteriosclerosis Through Inhibition of Vascular Smooth Muscle Cell Inflammatory Response to IFNγ

Qin

Wang

Xin

2019

The Anatomical Record

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IFNγ-induced vascular smooth muscle cells (VSMCs) inflammatory response plays a key role in transplant arteriosclerosis (TA). However, the mechanisms regulating this process remains poorly defined. Here, we show that ASK1-interacting protein 1 (AIP1) deletion markedly augments the expression of IFNγ-induced chemokines in mouse aortic allografts. Subsequently, donor arterial grafts from AIP1 deficient mice exhibited an accelerated development of TA. Furthermore, AIP1 knockdown significantly increased IFNγ signaling activation in cultured VSMCs and thus enhances chemokines production in response to IFNγ. Together, we conclude that AIP1 functions as an inhibitor of VSMCs inflammation by regulating IFNγ signaling and therefore suppresses TA progression. Our findings suggest that AIP1 might be a potential therapeutic target for chronic transplant rejection.

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ASK family in cardiovascular biology and medicine

Cited by 12 publications

References 93 publications

Metformin influences drug sensitivity in pancreatic cancer cells

Metformin influences drug sensitivity in pancreatic cancer cells

Psychological Stress and Cellular Aging in Cancer: A Meta-Analysis

AIP1 Suppresses Transplant Arteriosclerosis Through Inhibition of Vascular Smooth Muscle Cell Inflammatory Response to IFNγ

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