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 recurre...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.展开更多
Since the publication of this article,we noticed a minor mistake in the article that needs to be corrected.We have checked the original data;the correct data are provided in this Corrigendum as follows.The key finding...Since the publication of this article,we noticed a minor mistake in the article that needs to be corrected.We have checked the original data;the correct data are provided in this Corrigendum as follows.The key findings of the article are not affected by these corrections.展开更多
基金The Science and Technology Innovation Program of Hunan Province[2022RC3072(Y.Tao)].
文摘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.
文摘Since the publication of this article,we noticed a minor mistake in the article that needs to be corrected.We have checked the original data;the correct data are provided in this Corrigendum as follows.The key findings of the article are not affected by these corrections.
