Human fortilin is a molecular target of dihydroartemisinin

Fujita, Takayuki; Felix, Kumar; Pinkaew, Decha; Hutadilok‐Towatana, Nongporn; Liu, Zhihe; Fujise, Kenichi

doi:10.1016/j.febslet.2008.02.055

Cited by 49 publications

(38 citation statements)

References 16 publications

(25 reference statements)

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“…Three kinds of drugs (DHA, sertraline and thioridazine) were reported as the direct anti-cancer drug targets for TCTP. Fujita et al demonstrated that DHA could bind to human TCTP and decrease its cellular level through promoting ubiquitination and proteasomedependent degradation (Fujita et al, 2008;Lucibello et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Targeted Efficacy of Dihydroartemisinin for Translationally Controlled Protein Expression in a Lung Cancer Model

Liu

Wu²,

Guo³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Objective: Lung cancer is one of the malignant tumors with greatest morbidity and mortality around the world. The keys to targeted therapy are discovery of lung cancer biomarkers to facilitate improvement of survival and quality of life for the patients with lung cancer. Translationally controlled tumor protein (TCTP) is one of the most overexpressed proteins in human lung cancer cells by comparison to the normal cells, suggesting that it might be a good biomarker for lung cancer. Materials and Methods: In the present study, the targeted efficacy of dihydroartemisinin (DHA) on TCTP expression in the A549 lung cancer cell model was explored. Results and Conclusions: DHA could inhibit A549 lung cancer cell proliferation, and simultaneously up-regulate the expression of TCTP mRNA, but down-regulate its protein expression in A549 cells. In addition, it promoted TCTP protein secretion. Therefore, TCTP might be used as a potential biomarker and therapeutic target for non-small cell lung cancers.

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Section: Discussionmentioning

confidence: 99%

Targeted Efficacy of Dihydroartemisinin for Translationally Controlled Protein Expression in a Lung Cancer Model

Liu

Wu²,

Guo³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Artemisinin not only displays antimalarial activity but was also found to be a potent anticancer agent in cellular assay (review in Efferth 2005), and screening for potential targets in this context has confirmed that TCTP is indeed a target for this drug (Efferth 2005(Efferth , 2006. The interaction of artemisinin with TCTP was then studied in cancer cells, and it was found that drug treatment results in degradation of TCTP (fortilin) via the ubiquitin-proteasome pathway (Fujita et al 2008). More recent publications described proof-of-principle investigations for the use of artemisinin as an anticancer drug in cellular models of lung cancer , of Neurofibromatosis type 1 (NF1)-associated tumours (Kobayashi et al 2014) and of breast cancer (Lucibello et al 2015).…”

Section: Tctp As An Anticancer Targetmentioning

confidence: 99%

The Translational Controlled Tumour Protein TCTP: Biological Functions and Regulation

Bommer

2017

Results and Problems in Cell Differentiation

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The Translational Controlled Tumour Protein TCTP (gene symbol TPT1, also called P21, P23, Q23, fortilin or histamine-releasing factor, HRF) is a highly conserved protein present in essentially all eukaryotic organisms and involved in many fundamental cell biological and disease processes. It was first discovered about 35 years ago, and it took an extended period of time for its multiple functions to be revealed, and even today we do not yet fully understand all the details. Having witnessed most of this history, in this chapter, I give a brief overview and review the current knowledge on the structure, biological functions, disease involvements and cellular regulation of this protein. TCTP is able to interact with a large number of other proteins and is therefore involved in many core cell biological processes, predominantly in the response to cellular stresses, such as oxidative stress, heat shock, genotoxic stress, imbalance of ion metabolism as well as other conditions. Mechanistically, TCTP acts as an anti-apoptotic protein, and it is involved in DNA-damage repair and in cellular autophagy. Thus, broadly speaking, TCTP can be considered a cytoprotective protein. In addition, TCTP facilitates cell division through stabilising the mitotic spindle and cell growth through modulating growth signalling pathways and through its interaction with the proteosynthetic machinery of the cell. Due to its activities, both as an anti-apoptotic protein and in promoting cell growth and division, TCTP is also essential in the early development of both animals and plants. Apart from its involvement in various biological processes at the cellular level, TCTP can also act as an extracellular protein and as such has been involved in modulating whole-body defence processes, namely in the mammalian immune system. Extracellular TCTP, typically in its dimerised form, is able to induce the release of cytokines and other signalling molecules from various types of immune cells. There are also several examples, where TCTP was shown to be involved in antiviral/antibacterial defence in lower animals. In plants, the protein appears to have a protective effect against phytotoxic stresses, such as flooding, draught, too high or low temperature, salt stress or exposure to heavy metals. The finding for the latter stress condition is corroborated by earlier reports that TCTP levels are considerably up-regulated upon exposure of earthworms to high levels of heavy metals. Given the involvement of TCTP in many biological processes aimed at maintaining cellular or whole-body homeostasis, it is not surprising that dysregulation of TCTP levels may promote a range of disease processes, foremost cancer. Indeed a large body of evidence now supports a role of TCTP in at least the most predominant types of human cancers. Typically, this can be ascribed to both the anti-apoptotic activity of the protein and to its function in promoting cell growth and division. However, TCTP also appears to be involved in the later stages of cancer progression, such ...

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“…Recently, certain artemisinin derivatives, especially dihydroartemisinin (DHA), were shown to have anticancer eVects in a wide variety of cancer models in vitro and in vivo, including breast cancer (Singh and Lai 2001), cervical cancer (Chen et al 2003), ovarian cancer (Chen et al 2003;Jiao et al 2007), glioma (Huang et al 2007), lung cancer (Mu et al 2008), leukemia (Singh and Lai 2005), Wbrosarcoma (Singh and Lai 2004), osteosarcoma (Fujita et al 2008), oral cancer (Nam et al 2007) and hepatoma (Hou et al 2008). The mechanisms of action for their antitumor activities are not fully understood, but may include induction of G 0 /G 1 cell cycle arrest (Hou et al 2008;EVerth et al 2003), increased apoptosis (Singh and Lai 2001;Jiao et al 2007;Huang et al 2007;Mu et al 2008;Singh and Lai 2004;Fujita et al 2008;Nam et al 2007;Hou et al 2008), inhibition of angiogenesis and lymphangiogenesis (Chen et al 2003;Wu et al 2006;Wang et al 2007), and increased sensitization to radiation and anticancer drugs (Singh and Lai 2001;Kim et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Growth inhibitory effects of dihydroartemisinin on pancreatic cancer cells: involvement of cell cycle arrest and inactivation of nuclear factor-κB

Chen

Sun

Wang

et al. 2009

J Cancer Res Clin Oncol

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Human fortilin is a molecular target of dihydroartemisinin

Cited by 49 publications

References 16 publications

Targeted Efficacy of Dihydroartemisinin for Translationally Controlled Protein Expression in a Lung Cancer Model

Targeted Efficacy of Dihydroartemisinin for Translationally Controlled Protein Expression in a Lung Cancer Model

The Translational Controlled Tumour Protein TCTP: Biological Functions and Regulation

Growth inhibitory effects of dihydroartemisinin on pancreatic cancer cells: involvement of cell cycle arrest and inactivation of nuclear factor-κB

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