Asset Details
Do you wish to reserve the book?
MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling
Do you wish to request the book?
MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling
2022
Overview
The incidence of cutaneous melanoma (CM) has been increasing annually worldwide. In this study, we identify that MrgprF, a MAS related GPR family member, is decreased in cutaneous melanoma tissues and cell lines due to hypermethylation of its promoter region, and show that patients with CM expressing high levels of MrgprF exhibit an improved clinical outcome. We demonstrate that MrgprF forced expression inhibits tumor cell proliferation, migration, xenograft tumor growth, and metastasis. On the contrary, MrgprF knockdown promotes tumor cell proliferation and transformation of immortalized human keratinocyte-HaCaT cells, supporting the inhibitory role of MrgprF during tumor progression. Mechanistic studies reveal that MrgprF reduces the phosphoinositol‑3‑kinase (PI3K) complex formation between p101 and p110γ subunits, the critical step for phosphatidylinositol-(3, 4)-P2 (PIP2) conversion to phosphatidylinositol-(3, 4, 5)-P3 (PIP3), and then reduces the activation of PI3K/Akt signaling. This effect can be reversed by Akt specific agonist SC79. In addition, AMG 706, a previously documented inhibitor for endothelial cell proliferation, is identified as a potential agonist for MrgprF, and can impede tumor growth both in vitro and in vivo. Taken together, our findings suggest that MrgprF, a novel tumor suppressor in cutaneous melanoma, may be useful as a therapeutic target in the future.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
1-Phosphatidylinositol 3-kinase
/ 692/4017
/ Agonists
/ Humans
/ Kinases
/ Medicine
/ Melanoma
/ Melanoma, Cutaneous Malignant
/ Oncology
/ Phosphatidylinositol 3,4,5-triphosphate
/ Phosphatidylinositol 3-Kinases - genetics
/ Phosphatidylinositol 3-Kinases - metabolism
/ Phosphatidylinositol 4,5-diphosphate
/ Proto-Oncogene Proteins c-akt - genetics
/ Proto-Oncogene Proteins c-akt - metabolism
/ Tumors
