Evidence map›Paper›PMID 37714844›Full record

ArticleNature communications2023

Activation of melanocortin-1 receptor signaling in melanoma cells impairs T cell infiltration to dampen antitumor immunity.

Yazhong Cui, Yang Miao, Longzhi Cao, Lifang Guo, Yue Cui, Chuanzhe Yan, Zhi Zeng, Mo Xu, Ting Han

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 42 citations in OpenAlex.

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  8. Late-Stage Serine Modification Enables Noncanonical Peptide Synthesis.Journal of the American Chemical Society · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Yazhong Cui *Graduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, 100730, Beijing, China.
Yang Miao *National Institute of Biological Sciences, 102206, Beijing, China.
Longzhi CaoGraduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, 100730, Beijing, China.
Lifang GuoDepartment of Thoracic Surgery, Beijing Chaoyang Hospital, Capital Medical University, 100020, Beijing, China.
Yue CuiNational Institute of Biological Sciences, 102206, Beijing, China.
Chuanzhe YanNational Institute of Biological Sciences, 102206, Beijing, China.
Zhi ZengGraduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, 100730, Beijing, China.ORCID http://orcid.org/0000-0003-4224-2860
Mo XuGraduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, 100730, Beijing, China. xumo@nibs.ac.cn.ORCID http://orcid.org/0009-0002-5202-6424
Ting HanGraduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, 100730, Beijing, China. hanting@nibs.ac.cn.ORCID http://orcid.org/0000-0003-3168-8699
Chinese Academy of Medical Sciences & Peking Union Medical College · CNCapital Medical University · CNNational Institute of Biological Sciences, Beijing · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibition of T cell infiltration dampens antitumor immunity and causes resistance to immune checkpoint blockade (ICB) therapy. By in vivo CRISPR screening in B16F10 melanoma in female mice, here we report that loss of melanocortin-1 receptor (MC1R) in melanoma cells activates antitumor T cell response and overcomes resistance to ICB. Depletion of MC1R from another melanocytic melanoma model HCmel1274 also enhances ICB efficacy. By activating the GNAS-PKA axis, MC1R inhibits interferon-gamma induced CXCL9/10/11 transcription, thus impairing T cell infiltration into the tumor microenvironment. In human melanomas, high MC1R expression correlates with reduced CXCL9/10/11 expression, impaired T cell infiltration, and poor patient prognosis. Whereas MC1R activation is restricted to melanoma, GNAS activation by hotspot mutations is observed across diverse cancer types and is associated with reduced CXCL9/10/11 expression. Our study implicates MC1R as a melanoma immunotherapy target and suggests GNAS-PKA signaling as a pan-cancer oncogenic pathway inhibiting antitumor T cell response.

Indexed as

MelanomaReceptor, Melanocortin, Type 1AnimalsClustered Regularly Interspaced Short Palindromic RepeatsFemaleHumansMiceSignal TransductionT-LymphocytesTumor MicroenvironmentReceptor, Melanocortin, Type 1

Identifiers

PMID37714844
PMCPMC10504282
OpenAlexW4386764959

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.