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Surgery Today
Erschienen in: Surgery Today 9/2016

29.10.2015 | Review Article

DNA damage response and sphingolipid signaling in liver diseases

verfasst von: Masayuki Nagahashi, Yasunobu Matsuda, Kazuki Moro, Junko Tsuchida, Daiki Soma, Yuki Hirose, Takashi Kobayashi, Shin-ichi Kosugi, Kazuaki Takabe, Masaaki Komatsu, Toshifumi Wakai

Erschienen in: Surgery Today | Ausgabe 9/2016

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Abstract

Patients with unresectable hepatocellular carcinoma (HCC) cannot generally be cured by systemic chemotherapy or radiotherapy due to their poor response to conventional therapeutic agents. The development of novel and efficient targeted therapies to increase their treatment options depends on the elucidation of the molecular mechanisms that underlie the pathogenesis of HCC. The DNA damage response (DDR) is a network of cell-signaling events that are triggered by DNA damage. Its dysregulation is thought to be one of the key mechanisms underlying the generation of HCC. Sphingosine-1-phosphate (S1P), a lipid mediator, has emerged as an important signaling molecule that has been found to be involved in many cellular functions. In the liver, the alteration of S1P signaling potentially affects the DDR pathways. In this review, we explore the role of the DDR in hepatocarcinogenesis of various etiologies, including hepatitis B and C infection and non-alcoholic steatohepatitis. Furthermore, we discuss the metabolism and functions of S1P that may affect the hepatic DDR. The elucidation of the pathogenic role of S1P may create new avenues of research into therapeutic strategies for patients with HCC.
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Metadaten
Titel
DNA damage response and sphingolipid signaling in liver diseases
verfasst von
Masayuki Nagahashi
Yasunobu Matsuda
Kazuki Moro
Junko Tsuchida
Daiki Soma
Yuki Hirose
Takashi Kobayashi
Shin-ichi Kosugi
Kazuaki Takabe
Masaaki Komatsu
Toshifumi Wakai
Publikationsdatum
29.10.2015
Verlag
Springer Japan
Erschienen in
Surgery Today / Ausgabe 9/2016
Print ISSN: 0941-1291
Elektronische ISSN: 1436-2813
DOI
https://doi.org/10.1007/s00595-015-1270-8

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