Tenovin-6 induces the SIRT-independent cell growth suppression and blocks autophagy flux in canine hemangiosarcoma cell lines

Igase, Masaya; Fujiki, Noriyuki; Shibutani, Shusaku; Sakai, Hiroki; Noguchi, Shunsuke; Nemoto, Yasuhiro; Mizuno, Takuya

doi:10.1016/j.yexcr.2019.111810

Cited by 13 publications

(8 citation statements)

References 38 publications

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“…apoptosis or autophagy (Carafa et al, 2018(Carafa et al, , 2019De et al, 2018;Tae et al, 2018Tae et al, , 2020Igase et al, 2020).…”

Section: Efficiency Of Hdacimentioning

confidence: 99%

“…HDACi can also induce DNA damage, cell cycle arrest, apoptosis and autophagy to promote cancer cell death mentioned above. Some novel SIRT inhibitors, such as MC2494, MHY2245, MHY2256, tenovin-6, and YC8-02, also perform diverse anti-tumor activities through mediating apoptosis or autophagy ( Carafa et al, 2018 , 2019 ; De et al, 2018 ; Tae et al, 2018 , 2020 ; Li M. et al, 2019 ; Igase et al, 2020 ).…”

Section: Hdac Inhibitors In Cancer Therapymentioning

confidence: 99%

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The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy

Guo

Tian

Zhu

2020

Front. Cell Dev. Biol.

199

135

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Genetic mutations and abnormal gene regulation are key mechanisms underlying tumorigenesis. Nucleosomes, which consist of DNA wrapped around histone cores, represent the basic units of chromatin. The fifth amino group (N ε) of histone lysine residues is a common site for post-translational modifications (PTMs), and of these, acetylation is the second most common. Histone acetylation is modulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs), and is involved in the regulation of gene expression. Over the past two decades, numerous studies characterizing HDACs and HDAC inhibitors (HDACi) have provided novel and exciting insights concerning their underlying biological mechanisms and potential anti-cancer treatments. In this review, we detail the diverse structures of HDACs and their underlying biological functions, including transcriptional regulation, metabolism, angiogenesis, DNA damage response, cell cycle, apoptosis, protein degradation, immunity and other several physiological processes. We also highlight potential avenues to use HDACi as novel, precision cancer treatments.

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“…apoptosis or autophagy (Carafa et al, 2018(Carafa et al, , 2019De et al, 2018;Tae et al, 2018Tae et al, , 2020Igase et al, 2020).…”

Section: Efficiency Of Hdacimentioning

confidence: 99%

Section: Hdac Inhibitors In Cancer Therapymentioning

confidence: 99%

The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy

Guo

Tian

Zhu

2020

Front. Cell Dev. Biol.

199

135

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“…Interestingly, some classical pharmaceutical molecules can also resist tumors by activating incomplete autophagy. The study found that tenovin‐6, a potent p53 activator, activates the SIRT‐independent cell growth inhibition and induces incomplete autophagy in canine hemangiosarcoma cell lines 150 . Dipyridamole is a vasodilator and antithrombotic drug that induces incomplete autophagy and exerts cytotoxicity on prostate cancer cells 151 .…”

Section: Implications Of Incomplete Autophagy For Pharmacotherapymentioning

confidence: 99%

“…The study found that tenovin-6, a potent p53 activator, activates the SIRT-independent cell growth inhibition and induces incomplete autophagy in canine hemangiosarcoma cell lines. 150 Dipyridamole is a vasodilator and antithrombotic drug that induces incomplete autophagy and exerts cytotoxicity on prostate cancer cells. 151 Trifluoperazine and salinomycin inhibit cell growth in melanoma by disrupting autophagy flux.…”

Section: Cancermentioning

confidence: 99%

Incomplete autophagy: Trouble is a friend

Zhang

Cao

Qiu

et al. 2022

Medicinal Research Reviews

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Incomplete autophagy is an impaired self‐eating process of intracellular macromolecules and organelles in which accumulated autophagosomes do not fuse with lysosomes for degradation, resulting in the blockage of autophagic flux. In this review, we summarized the literature over the past decade describing incomplete autophagy, and found that different from the double‐edged sword effect of general autophagy on promoting cell survival or death, incomplete autophagy plays a crucial role in disrupting cellular homeostasis, and promotes only cell death. What matters is that incomplete autophagy is closely relevant to the pathogenesis and progression of various human diseases, which, meanwhile, intimately linking to the pharmacologic and toxicologic effects of several compounds. Here, we comprehensively reviewed the latest progress of incomplete autophagy on molecular mechanisms and signaling pathways. Moreover, implications of incomplete autophagy for pharmacotherapy are also discussed, which has great relevance for our understanding of the distinctive role of incomplete autophagy in cellular physiology and disease. Consequently, targeting incomplete autophagy may contribute to the development of novel generation therapeutic agents for diverse human diseases.

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“…Despite its effective SIRT1 and SIRT2 inhibition, Tenovin-6 may target other proteins in cells. For instance, Tenovin-6 impaired cellular growth of canine hemangiosarcoma cells through a SIRT1-independent mechanism ( Igase et al, 2020 ). Tenovin-6’s effect in DLBCL cells is also thought to be SIRT1/2/3 independent ( Yuan et al, 2017 ).…”

Section: Overview Of Sirtuin Modulatorsmentioning

confidence: 99%

Sirtuin Modulators in Cellular and Animal Models of Human Diseases

Hong

Lin

2021

Front. Pharmacol.

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Sirtuins use NAD+ to remove various acyl groups from protein lysine residues. Through working on different substrate proteins, they display many biological functions, including regulation of cell proliferation, genome stability, metabolism, and cell migration. There are seven sirtuins in humans, SIRT1-7, each with unique enzymatic activities, regulatory mechanisms, subcellular localizations, and substrate scopes. They have been indicated in many human diseases, including cancer, neurodegeneration, microbial infection, metabolic and autoimmune diseases. Consequently, interests in development of sirtuin modulators have increased in the past decade. In this brief review, we specifically summarize genetic and pharmacological modulations of sirtuins in cancer, neurological, and cardiovascular diseases. We further anticipate this review will be helpful for scrutinizing the significance of sirtuins in the studied diseases.

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Tenovin-6 induces the SIRT-independent cell growth suppression and blocks autophagy flux in canine hemangiosarcoma cell lines

Cited by 13 publications

References 38 publications

The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy

The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy

Incomplete autophagy: Trouble is a friend

Sirtuin Modulators in Cellular and Animal Models of Human Diseases

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