Neural stem cells inhibit melanin production by activation of Wnt inhibitors

Hwang, Inhwa; Park, Ju Hwang; Park, Hang-Soo; Choi, Kyung Ah; Seol, Ki Cheon; Oh, Seung Ick; Kang, Seongman; Hong, Sunghoi

doi:10.1016/j.jdermsci.2013.08.006

Cited by 29 publications

(34 citation statements)

References 45 publications

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“…Independently of its effect on GLI2, TGFβ inhibits PKA that otherwise promotes CREB-dependent MITF transcription [ 68 ]. DKK1 (Dickkopf-1), a secreted inhibitor of the Wnt/β-catenin pathway, has been shown to suppress both MITF expression and the MITF-dependent differentiation program [ 78 ]. Accordingly, both DKK1 expression and secretion have been substantially reduced in the multicellular anchorage-independent melanospheres showing high expression of MITF and numerous MITF target genes [ 79 ].…”

Section: Gene Structure and Transcriptional Regulation Of Mmentioning

confidence: 99%

MITF in melanoma: mechanisms behind its expression and activity

Hartman

Czyż

2014

Cell. Mol. Life Sci.

249

235

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MITF (microphthalmia-associated transcription factor) represents a melanocytic lineage-specific transcription factor whose role is profoundly extended in malignant melanoma. Over the last few years, the function of MITF has been tightly connected to plasticity of melanoma cells. MITF participates in executing diverse melanoma phenotypes defined by distinct gene expression profiles. Mutation-dependent alterations in MITF expression and activity have been found in a relatively small subset of melanomas. MITF activity is rather modulated by its upstream activators and suppressors operating on transcriptional, post-transcriptional and post-translational levels. These regulatory mechanisms also include epigenetic and microenvironmental signals. Several transcription factors and signaling pathways involved in the regulation of MITF expression and/or activity such as the Wnt/β-catenin pathway are broadly utilized by various types of tumors, whereas others, e.g., BRAFV600E/ERK1/2 are more specific for melanoma. Furthermore, the MITF activity can be affected by the availability of transcriptional co-partners that are often redirected by MITF from their own canonical signaling pathways. In this review, we discuss the complexity of a multilevel regulation of MITF expression and activity that underlies distinct context-related phenotypes of melanoma and might explain diverse responses of melanoma patients to currently used therapeutics.

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Section: Gene Structure and Transcriptional Regulation Of Mmentioning

confidence: 99%

MITF in melanoma: mechanisms behind its expression and activity

Hartman

Czyż

2014

Cell. Mol. Life Sci.

249

235

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“…In our previous study, NSC‐CM inhibited melanin production by activating Wnt inhibitors, and another group reported that NSC‐CM increased total tubule formation of human umbilical vein endothelial cells . However, to our knowledge, NSC‐CM has not been investigated for the reduction of stem cell‐derived teratomas or other tumors.…”

Section: Discussionmentioning

confidence: 96%

“…Recently, the ability of conditioned medium (CM) from many different stem cell types have been shown to trigger cancer cell death, including: human adipose stromal cell‐derived CM induced cancer cell death in vitro, human umbilical cord mesenchymal stem cell‐derived CM induced apoptosis of cholangiocarcinoma cells, and mesenchymal stem cell‐derived CM inhibited the growth and promoted the apoptosis of hepatoma cells . In our previous study showing the paracrine effects of neural stem cell‐derived CM (NSC‐CM) on the inhibition of melanin production in the B16 melanoma cancer cell line, we observed that a high concentration of NSC‐CM triggered morphological changes and reduced cell proliferation of the B16 cell line. Therefore, based on these results, we hypothesized that CM treatment inhibits the growth of teratomas from contaminating PSCs within a population of fully differentiated tissue‐specific cells after transplantation.…”

Section: Introductionmentioning

confidence: 99%

Tissue inhibitor of metalloproteinase proteins inhibit teratoma growth in mice transplanted with pluripotent stem cells

et al. 2019

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Pluripotent stem cells (PSCs) can serve as an unlimited cell source for transplantation therapies for treating various devastating diseases, such as cardiovascular diseases, diabetes, and Parkinson's disease. However, PSC transplantation has some associated risks, including teratoma formation from the remaining undifferentiated PSCs. Thus, for successful clinical application, it is essential to ablate the proliferative PSCs before or after transplantation. In this study, neural stem cell‐derived conditioned medium (NSC‐CM) inhibited the proliferation of PSCs and PSC‐derived neural precursor (NP) cells without influencing the potential of PSC‐NP cells to differentiate into neurons in vitro and prevented teratoma growth in vivo. Moreover, we found that the NSC‐CM remarkably decreased the expression levels of Oct4 and cyclin D1 that Oct4 directly binds to and increased the cleaved‐caspase 3‐positive cell death through the DNA damage response in PSCs and PSC‐NPs. Interestingly, we found that NSCs distinctly secreted the tissue inhibitor of metalloproteinase (TIMP)‐1 and TIMP‐2 proteins. These proteins suppressed not only the proliferation of PSCs in cell culture but also teratoma growth in mice transplanted with PSCs through inhibition of matrix metalloproteinase (MMP)‐2 and MMP‐9 activity. Taken together, these results suggest that the TIMP proteins may improve the efficacy and safety of the PSC‐based transplantation therapy.

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“…Wnt signaling pathway. The Wnt signaling pathway has been previously reported to serve an important role in melanogenesis (24,25). Wnt ligands bind to Frizzled receptors on the cell surface, resulting in the increased stability of cytoplasmic β-catenin, and its subsequent translocation into the nucleus, where it activates the transcription of MITF by interplay with lymphoid enhancer-binding factor 1 (LEF1)/T-cell factor (LEF1/TCF) (26).…”

Section: Core Signaling Pathways In the Regulation Of Melanogenesismentioning

confidence: 99%

Natural skin‑whitening compounds for the treatment of melanogenesis (Review)

et al. 2020

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Melanogenesis is the process for the production of melanin, which is the primary cause of human skin pigmentation. Skin-whitening agents are commercially available for those who wish to have a lighter skin complexions. To date, although numerous natural compounds have been proposed to alleviate hyperpigmentation, insufficient attention has been focused on potential natural skin-whitening agents and their mechanism of action from the perspective of compound classification. In the present article, the synthetic process of melanogenesis and associated core signaling pathways are summarized. An overview of the list of natural skin-lightening agents, along with their compound classifications, is also presented, where their efficacy based on their respective mechanisms of action on melanogenesis is discussed.

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Neural stem cells inhibit melanin production by activation of Wnt inhibitors

Cited by 29 publications

References 45 publications

MITF in melanoma: mechanisms behind its expression and activity

MITF in melanoma: mechanisms behind its expression and activity

Tissue inhibitor of metalloproteinase proteins inhibit teratoma growth in mice transplanted with pluripotent stem cells

Natural skin‑whitening compounds for the treatment of melanogenesis (Review)

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