FFAR1-and FFAR4-dependent activation of Hippo pathway mediates DHA-induced apoptosis of androgen-independent prostate cancer cells

Wang, Jingzhao; Hong, Yuheng; Shao, Shuai; Zhang, Kun; Wang, Hong

doi:10.1016/j.bbrc.2018.10.088

Cited by 21 publications

(16 citation statements)

References 24 publications

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“…An animal study showed that mimicking MYC overexpression induces PCa progression in PCa-model mice fed a diet high in saturated fatty acids [37]. However, suppression of PCa cell proliferation by intake of unsaturated fatty acids, such as eicosapentaenoic acids, docosahexaenoic acids, and α-linolenic acids, was demonstrated in an animal study and several in vitro experiments using human PCa cell lines [38][39][40][41].…”

Section: Fatmentioning

confidence: 99%

Influence of Diet and Nutrition on Prostate Cancer

Matsushita

Fujita

Nonomura

2020

IJMS

119

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The incidence of prostate cancer (PCa) displays widespread regional differences, probably owing to differences in dietary habits. Nutrients, including fat, protein, carbohydrates, vitamins (vitamin A, D, and E), and polyphenols, potentially affect PCa pathogenesis and progression, as previously reported using animal models; however, clinical studies have reported controversial results for almost all nutrients. The effects of these nutrients may be manifested through various mechanisms including inflammation, antioxidant effects, and the action of sex hormones. Dietary patterns including the Western and Prudent patterns also influence the risk of PCa. Recent studies reported that the gut microbiota contribute to tumorigenesis in some organs. Diet composition and lifestyle have a direct and profound effect on the gut bacteria. Human studies reported an increase in the abundance of specific gut bacteria in PCa patients. Although there are few studies concerning their relationship, diet and nutrition could influence PCa, and this could be mediated by gut microbiota. An intervention of dietary patterns could contribute to the prevention of PCa. An intervention targeting dietary patterns may thus help prevent PCa.

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Section: Fatmentioning

confidence: 99%

Influence of Diet and Nutrition on Prostate Cancer

Matsushita

Fujita

Nonomura

2020

IJMS

119

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“…The inhibition of Yap expression can activate breast cancer cell apoptosis; and in cardiac reperfusion injury, the Yap-Hippo pathway is inhibited and contributes to the progression of cardiac dysfunction by augmenting cardiomyocytes [66]. Moreover, in prostate cancer, Yap activation modulates docosahexaenoic acid-induced apoptosis in a manner dependent on the FFAR4 pathway [67]. Notably, the beneficial effects of Yap in brain tissues have also been widely explored.…”

Section: Discussionmentioning

confidence: 99%

Mitofusin-2 regulates inflammation-mediated mouse neuroblastoma N2a cells dysfunction and endoplasmic reticulum stress via the Yap-Hippo pathway

2019

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Endoplasmic reticulum (ER) stress is involved in inflammation-induced neurotoxicity. Mitofusin 2 (Mfn2), a member of the GTPase family of proteins, resides in the ER membrane and is known to regulate ER stress. However, the potential role and underlying mechanism of Mfn2 in inflammation-induced neuronal dysfunction is unknown. In our study, we explored the potential of Mfn2 to attenuate inflammation-mediated neuronal dysfunction by inhibiting ER stress. Our data show that Mfn2 overexpression significantly ameliorated tumor necrosis factor alpha (TNFα)-induced ER stress, as indicated by the downregulation of the ER stress proteins PERK, GRP78 and CHOP. Mfn2 overexpression also prevented the TNFα-mediated activation of caspase-3, caspase-12 and cleaved poly (ADP-ribose) polymerase (PARP). Cellular antioxidant dysfunction and reactive oxygen species overproduction were also improved by Mfn2 in the setting of TNFα in mouse neuroblastoma N2a cells in vitro. Similarly, disordered calcium homeostasis, indicated by disturbed levels of calcium-related proteins and calcium overloading, was corrected by Mfn2, as evidenced by the increased expression of store-operated calcium entry (SERCA), decreased levels of inositol trisphosphate receptor (IP3R), and normalized calcium content in TNFα-treated N2a cells. Mfn2 overexpression was found to elevate Yes-associated protein (Yap) expression; knockdown of Yap abolished the regulatory effects of Mfn2 on ER stress, oxidative stress, calcium balance, neural death and inflammatory injury. These results lead us to conclude that re-activation of the Mfn2-Yap signaling pathway alleviates TNFα-induced ER stress and dysfunction of mouse neuroblastoma N2a cells. Our findings provide a better understanding of the regulatory role of Mfn2-Yap-ER stress in neuroinflammation and indicate that the Mfn2-Yap axis may be a focus of research in terms of having therapeutic value for the treatment of neurodegenerative diseases.

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“…YAP1/TAZ is generally activated by Gα12/13, Gα q/11 , and Gα i ; these G proteins are coupled with different GPCRs, including lysophosphatidic acid receptors, sphingosine1-phosphate (S1P) receptors, and protease-activated receptor 1 [73][74][75][76][77][78][79]. However, Gα s inhibits the Hippo-YAP1/TAZ pathway by other GPCRs, such as free fatty acid receptor 1/4 (FFAR1/4, also called as G-protein receptor 40/120 [GPR40/120]) [80][81][82]. Gα 12/13 , Gα q/11 , and Gα i mainly upregulate Ras homology family member A (RhoA)-Rho associated protein kinase (ROCK) signaling to catalyze the phosphorylation of its substrates, which affects YAP1/TAZ.…”

Section: Interaction Of Hippo-yap1/taz Signaling With the Gpcr Pathwaymentioning

confidence: 99%

Section: Interaction Of Hippo-yap1/taz Signaling With the Gpcr Pathwamentioning

confidence: 99%

“…Paradoxically, PKs, together with Gα s , impairs the activity of YAP1/TAZ. In combination with Gα s , FFAR1/2/4 activates PKA-induced phosphorylation of MST1/LATS1; thereafter, YAP1 is phosphorylated and detained in the cytoplasm, which inhibits cell proliferation and cell metastasis, and induces apoptosis of tumor cells 80 - 82 . Notably, the Gα s -PKA-induced suppression of YAP1 can be disrupted by positive G proteins, including Gα 12/13 , Gα q/11 , and Gα i 95 .…”

Section: Interaction Of Hippo-yap1/taz Signaling With the Gpcr Pathwamentioning

confidence: 99%

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Role of Hippo-YAP1/TAZ pathway and its crosstalk in cardiac biology

Chen¹,

Yuan²,

Li³

et al. 2020

Int. J. Biol. Sci.

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The Hippo pathway undertakes a pivotal role in organ size control and the process of physiology and pathology in tissue. Its downstream effectors YAP1 and TAZ receive upstream stimuli and exert transcription activity to produce biological output. Studies have demonstrated that the Hippo pathway contributes to maintenance of cardiac homeostasis and occurrence of cardiac disease. And these cardiac biological events are affected by crosstalk among Hippo-YAP1/TAZ, Wnt/β-catenin, Bone morphogenetic protein (BMP) and G-protein-coupled receptor (GPCR) signaling, which provides new insights into the Hippo pathway in heart. This review delineates the interaction among Hippo, Wnt, BMP and GPCR pathways and discusses the effects of these pathways in cardiac biology.

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FFAR1-and FFAR4-dependent activation of Hippo pathway mediates DHA-induced apoptosis of androgen-independent prostate cancer cells

Cited by 21 publications

References 24 publications

Influence of Diet and Nutrition on Prostate Cancer

Influence of Diet and Nutrition on Prostate Cancer

Mitofusin-2 regulates inflammation-mediated mouse neuroblastoma N2a cells dysfunction and endoplasmic reticulum stress via the Yap-Hippo pathway

Role of Hippo-YAP1/TAZ pathway and its crosstalk in cardiac biology

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