Evidence map›Paper›PMID 36725837›Full record

ArticleSignal transduction and targeted therapy2023

GPR162 activates STING dependent DNA damage pathway as a novel tumor suppressor and radiation sensitizer.

Yao Long, Jiaxing Guo, Jielin Chen, Jingyue Sun, Haiyan Wang, Xin Peng, Zuli Wang, WeiWei Lai, Na Liu, Long Shu and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 1 institution in 2 countries.

Yao LongDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Jiaxing GuoDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Jielin ChenDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Jingyue SunDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Haiyan WangDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Xin PengDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.ORCID http://orcid.org/0000-0003-0601-4991
Zuli WangDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
WeiWei LaiDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Na LiuDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.ORCID http://orcid.org/0000-0001-5162-3791
Long ShuDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Ling ChenDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Ying ShiDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.ORCID http://orcid.org/0000-0003-4671-4896
Desheng XiaoDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China. xdsh96@csu.edu.cn.ORCID http://orcid.org/0000-0003-2204-5042
Shuang LiuDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China. shuangliu2016@csu.edu.cn.ORCID http://orcid.org/0000-0002-7206-7277
Yongguang TaoDepartment of Pathology, Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education), Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China. taoyong@csu.edu.cn.ORCID http://orcid.org/0000-0003-2354-5321
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the treatment of most malignancies, radiotherapy plays a significant role. However, the resistance of cancer cells to ionizing radiation (IR) is the main reason for the failure of radiotherapy, which causes tumor recurrence and metastasis. In this study, we confirmed that GPR162, an orphan receptor in the G-protein-coupled receptor family, acted as a novel radiotherapy sensitizer by interacting with the stimulator of interferon genes (STING), which targeted DNA damage responses, activated IRF3, accelerated the activation of type I interferon system, promoted the expression of chemokines including CXCL10 and CXCL4, and inhibited the occurrence and development of tumors. Interestingly, the activation of STING by overexpression of GPR162 was independent of the classical pathway of cGAS. STING inhibitors could resist the antitumor effect of overexpression of GPR162 in IR-induced mouse models. In addition, most solid tumors showed low expression of GPR162. And the higher expression of GPR162 indicated a better prognosis in patients with lung adenocarcinoma, liver cancer, breast cancer, etc. In summary, these results suggested that GPR162 may serve as a potential sensitizer of radiotherapy by promoting radiotherapy-induced STING-IFN production and increasing the expression of chemokines including CXCL10 and CXCL4 in DNA damage response, providing an alternative strategy for improving cancer radiotherapy.

Indexed as

Interferon Type INeoplasmsRadiation-Sensitizing AgentsAnimalsMiceSignal TransductionInterferon Type IRadiation-Sensitizing Agents

Identifiers

PMID36725837
PMCPMC9892510
OpenAlexW4318829783

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.