Related Experiment Video
Updated: Mar 17, 2026
06:09
Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
Published on: June 7, 2019
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Oncogenic GPR161 Drives Melanoma Proliferation and Metabolic Activity through TXNIP Inhibition
Yuna Roh1,2, Jinhyeon Choi1,3, Jin-Seong Hwang1
1Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea.
Journal of Microbiology and Biotechnology
|March 16, 2026
Summary
G-protein-coupled receptor 161 (GPR161) drives melanoma progression by activating signal transducer and activator of transcription 3 (STAT3) and suppressing thioredoxin-interacting protein (TXNIP), promoting cell growth and metabolic reprogramming. GPR161 is a potential therapeutic target for melanoma.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Melanoma progression involves oncogenic signaling and metabolic reprogramming.
- The role of G-protein-coupled receptors (GPCRs) in these processes is not well understood.
Purpose of the Study:
- To investigate the role of GPR161 in melanoma progression.
- To elucidate the regulatory mechanisms and downstream effects of GPR161 in melanoma.
Main Methods:
- Promoter analysis and ChIP-qPCR to assess STAT3 binding to GPR161.
- Functional studies involving GPR161 and STAT3 inhibition/silencing.
- Transcriptomic profiling to identify downstream targets.
- Analysis of Cancer Genome Atlas datasets.
Main Results:
- GPR161 is upregulated in melanoma and associated with poor survival.
- GPR161 promotes melanoma cell proliferation and migration.
- STAT3 directly activates GPR161 transcription, promoting melanoma growth.
- GPR161 negatively regulates TXNIP, enhancing glycolytic capacity and proliferation.
- A STAT3-GPR161-TXNIP axis was identified, with low TXNIP predicting poor survival.
Conclusions:
- GPR161 promotes melanoma malignancy by linking STAT3 activation to TXNIP suppression and metabolic enhancement.
- GPR161 represents a potential biomarker and therapeutic target for melanoma.
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