Basal and induced sphingosine kinase 1 activity in A549 carcinoma cells: function in cell survival and IL-1β and TNF-α induced production of inflammatory mediators

Billich, Andreas; Bornancin, Frédéric; Mechtcheriakova, Diana; Natt, François; Huesken, Dieter; Baumruker, Thomas

doi:10.1016/j.cellsig.2004.12.005

Cited by 132 publications

(115 citation statements)

References 52 publications

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“…Most likely, hypoxia causes an increase in SphK2 by achieving post-translational protein modification. However, the enhancing of mRNA transcription and translation or affecting mRNA stability is also possible [104][105][106] . The extracellular S1P activity leads to chemoresistance mediated via S1P1/S1P3 receptors and p42/44 MAPK-dependent signaling pathways as well 106 .…”

mentioning

confidence: 99%

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

Doktorova

Hraběta

Khalil

et al. 2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. The aim of this review is to provide the information about molecular basis of hypoxia-induced chemoresistance, focusing on the possibility of diagnostic and therapeutic use. Results. Hypoxia is a common feature of tumors and represents an independent prognostic factor in many cancers. It is the result of imbalances in the intake and consumption of oxygen caused by abnormal vessels in the tumor and the rapid proliferation of cancer cells. Hypoxia-induced resistance to cisplatin, doxorubicin, etoposide, melphalan, 5-flouoruracil, gemcitabine, and docetaxel has been reported in a number of experiments. Adaptation of tumor cells to hypoxia has important biological effects. The most studied factor responsible for these effects is hypoxia-inducible factor-1 (HIF-1) that significantly contributes to the aggressiveness and chemoresistance of different tumors. The HIF-1 complex, induced by hypoxia, binds to target genes, thereby increasing the expression of many genes. In addition, the expression of hundreds of genes can be also decreased in response to hypoxia in HIF-1 dependent manner, but without the detection of HIF-1 in these genes' promoters. HIF-1 independent mechanisms for drug resistance in hypoxia have been described, however, they are still rarely reported. The first clinical studies focusing on diagnosis of hypoxia and on inhibition of hypoxia-induced changes in cancer cells are starting to yield results. Conclusions. The adaptation to hypoxia requires many genetic and biochemical responses that regulate one another. Hypoxia-induced resistance is a very complex field and we still know very little about it. Different approaches to circumvent hypoxia in tumors are under development.

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mentioning

confidence: 99%

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

Doktorova

Hraběta

Khalil

et al. 2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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“…Blockage of SphK1 activity in an animal arthritis model indeed significantly suppressed articular inflammation and joint destruction, reduced disease severity, and down-regulated proinflammatory cytokine production and inflammatory cell infiltration into the synovium [49]. In fact, inhibition of S1P synthesis by blocking SphK activity has proven useful as an anti-inflammation strategy in cancer therapy [97][98][99][100][101].…”

Section: Targeting S1p Levelsmentioning

confidence: 99%

Sphingosine-1-Phosphate and Rheumatoid Arthritis: Pathological Implications and Potential Therapeutic Targets

Zhang¹,

Chang²

2013

Innovative Rheumatology

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“…Moreover Fumonisin B1 abrogates the proapoptotic effects of palmitate on L6 myotubes [78]. Inhibition of basal SphK1 activity, obtained by N,N-dimethylsphingosine, induces a spontaneous apoptosis in A549 carcinoma cells [66]. In contrast to pro-survival SphK1, the protein SphK2, a nuclear protein [79], inhibits cell growth and enhances apoptosis [80].…”

Section: Apoptosis and Cell Growthmentioning

confidence: 99%

“…The inhibition of basal SphK1 activity is obtained by N,N-dimethylsphingosine [65]. DL-threo-dihydrosphingosine, besides SphK1 inhibition, increases the sensitivity of HEK-293 cells to fumonisin B1, inhibitor of CerS [66]. While N,N-dimethyl-sphingosine displays inhibitory effects for both SphK1 and SphK2, synthetic sphingoid analogs, as SG12 and SG14, have specific inhibitory effects on SphK2 [67].…”

Section: Inhibitors Of Ceramide Utilizationmentioning

confidence: 99%

Sphingolipid Metabolism Inhibitors and Cell Function

Albi¹,

Magni²

2008

TOEIJ

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It has been widely shown that ceramide, ceramide phosphate, sphingosine and sphingosine-1-phosphate are molecules involved in cell proliferation, differentiation and apoptosis. The regulation of the enzymes that control their metabolism has an important role for cellular fate. Many studies in the field have shed light on sphingolipid metabolism inhibition and on its role in cell processes such as gene expression, DNA duplication and RNA transcription. The aim of this review is to collect, in a systematic way, the recent advances in the field of sphingolipid metabolism inhibitors, with special emphasis on their effects on cell function.

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Basal and induced sphingosine kinase 1 activity in A549 carcinoma cells: function in cell survival and IL-1β and TNF-α induced production of inflammatory mediators

Cited by 132 publications

References 52 publications

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

Sphingosine-1-Phosphate and Rheumatoid Arthritis: Pathological Implications and Potential Therapeutic Targets

Sphingolipid Metabolism Inhibitors and Cell Function

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