Transducin-like enhancer of split 3 regulates proliferation of melanoma cells via histone deacetylase activity

Honeybees produce royal jelly (RJ) from their cephalic glands. Royal jelly is a source of nutrition for the queen honey bee throughout its lifespan and is also involved in fertility and longevity. Royal jelly has long been considered beneficial to human health. We recently observed that RJ delayed impairment of motor function during aging, affecting muscle fiber size. However, how RJ affects skeletal muscle metabolism and the functional component of RJ is as of yet unidentified. We demonstrate that feeding mice with RJ daily prevents a decrease in myofiber size following denervation without affecting total muscle weight. RJ did not affect atrophy-related genes but stimulated the expression of myogenesis-related genes, including IGF-1 and IGF receptor. Trans-10-hydroxy-2-decenoic acid (10H2DA) and 10-hydroxydecanoic acid (10HDAA), two major fatty acids contained in RJ. After ingestion, 10H2DA and 10HDAA are metabolized into 2-decenedioic acid (2DA) and sebacic acid (SA) respectively. We found that 10H2DA, 10HDAA, 2DA, and SA all regulated myogenesis of C2C12 cells, murine myoblast cells. These novel findings may be useful for potential preventative and therapeutic applications for muscle atrophy disease included in Sarcopenia, an age-related decline in skeletal muscle mass and strength.

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“…Proliferation of C2C12 cells was assessed using a Cell Counting kit-8 (Dojindo, Kumamoto, Japan) according to the manufacturer’s protocol [ 39 ].…”

Section: Methodsmentioning

confidence: 99%

Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy

et al. 2020

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“…Empty adenovirus was infected at RAW 264.7 cells for 6 h. After infection, 5000 cells of adenovirus infected or non-infected RAW 264.7 cells were plated at 96 well plate. The cell viability was determined by Cell Counting Kit-8 (Dojindo, Kumamoto, Japan) by manufacturer protocol ( Ogawa et al, 2019 ). Cell viability was not affected by adenovirus infection (Fig.…”

Section: Methodsmentioning

confidence: 99%

Protein phosphatase 1 regulatory subunit 18 suppresses the transcriptional activity of NFATc1 via regulation of c-fos

et al. 2021

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The transcription factor NFATc1 and its binding partner AP-1 (a complex containing c-fos and c-Jun) play a central role in osteoclast differentiation. NFATc1 and AP-1 promote the expression of target genes such as Acp5, Ctsk and also auto-regulate NFATc1 expression as well. We previously reported that protein phosphatase 1 regulatory subunit 18 (PPP1r18) is a negative regulator of osteoclast bone resorption by inhibiting cell attachment to bone matrix. We also reported that PPP1r18 potentially regulates NFATc1 expression during osteoclast differentiation. To further explore this, in this study we have examined the effect of PPP1r18 on NFATc1 expression and activity by overexpressing PPP1r18 during the early stage of osteoclast differentiation. We found that PPP1r18 suppressed NFATc1 expression through inhibition of the transcriptional activity of NFATc1. Since PPP1r18 does not regulate NFATc1 directly, we next explored the involvement of AP-1. Our data showed that c-fos phosphorylation and nuclear localization were reduced by PPP1r18 overexpression. Further experiments showed that overexpression of c-fos together with PPP1r18 rescued NFATc1 expression and transcriptional activity. Moreover, c-fos activity inhibition by PPP1r18 was canceled by mutation of the phosphatase binding site of PPP1r18. Taken together, PPP1r18-regulated phosphatase activity targets c-fos phosphorylation and suppresses subsequent NFATc1 expression and activity.

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“…Tumors were then dissected, measured, and weighed. Volumes were calculated using a formula previously described 40 . 10 µm sections were prepared using a cryostat.…”

Section: Animals and Tumor Injectionmentioning

confidence: 99%

“…5,000 cells per well were plated in 96 well plates. Cell viability was assessed every 24 h with the Cell Counting Kit-8 (Dojindo, Kumamoto, Japan), according to the manufacturer's protocol 40 .…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

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Plectin Promotes Melanoma Tumor Formation by Regulation of Src Activity

Mizuta

Matsubara

Goto

et al. 2021

Preprint

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Melanoma is malignant cancer characterized by high proliferation and aggressive metastasis. To address efficient treatment for melanoma, we should understand the molecular mechanisms for a proto-oncogene Src, which is highly activated and promotes cell proliferation, migration, adhesion, and metastasis in melanoma. We recently identified plectin as the Src binding protein and regulates Src activity in osteoclasts. Plectin, a cytoskeleton regulatory protein, is focused as the candidates of biomarker of certain tumors because of higher expression and the candidate of anti-tumor reagents such as ruthenium pyridinecarbothioamide although the molecular mechanisms how plectin works in melanoma is unclear. In this study, we examined the pathological role in melanoma tumor formation. Depletion of plectin induced low density and sparce tumor formation by melanoma cells in vivo. In vitro experiment revealed that plectin deficient melanomas reduced cell proliferation and suppressed cell-to-cell adhesion. Because Src activity was reduced in plectin deficient melanomas, we examined the relationship between plectin and Src signaling. Src overexpression that restored Src activity rescued cell proliferation and cell-to-cell adhesion of plectin deficient melanomas. These results suggest that plectin is required for tumor formation by promoting cell proliferation and cell-to-cell adhesion via Src signaling activity in melanoma.

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Transducin-like enhancer of split 3 regulates proliferation of melanoma cells via histone deacetylase activity

Cited by 11 publications

References 42 publications

Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy

Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy

Protein phosphatase 1 regulatory subunit 18 suppresses the transcriptional activity of NFATc1 via regulation of c-fos

Plectin Promotes Melanoma Tumor Formation by Regulation of Src Activity

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