High expression of GPR160 in prostate cancer is unrelated to CARTp-mediated signaling pathways

Chenyu Ye¹, Qingtong Zhou^{1

2}, Shi Lin², Wensheng Yang³, Xiaoqing Cai^{4

5}, Yiting Mai², Yanyan Chen², Dehua Yang^{2

4

5

6}, Ming-Wei Wang^{1

2

7

8}

Affiliations

¹ Department of Pharmacology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
² Research Center for Deepsea Bioresources, Sanya 572025, China.
³ Department of Pharmacy, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai 201102, China.
⁴ State Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
⁵ The National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
⁶ University of Chinese Academy of Sciences, Beijing 100049, China.
⁷ Department of Chemistry, School of Science, the University of Tokyo, Tokyo 113-0033, Japan.
⁸ School of Pharmacy, Hainan Medical University, Haikou 571199, China.

PMID: 38487007
PMCID: PMC10935005
DOI: 10.1016/j.apsb.2023.11.025

High expression of GPR160 in prostate cancer is unrelated to CARTp-mediated signaling pathways

Chenyu Ye et al. Acta Pharm Sin B. 2024 Mar.

. 2024 Mar;14(3):1467-1471.

doi: 10.1016/j.apsb.2023.11.025. Epub 2023 Nov 24.

Authors

Chenyu Ye¹, Qingtong Zhou^{1

2}, Shi Lin², Wensheng Yang³, Xiaoqing Cai^{4

5}, Yiting Mai², Yanyan Chen², Dehua Yang^{2

4

5

6}, Ming-Wei Wang^{1

2

7

8}

Affiliations

¹ Department of Pharmacology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
² Research Center for Deepsea Bioresources, Sanya 572025, China.
³ Department of Pharmacy, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai 201102, China.
⁴ State Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
⁵ The National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
⁶ University of Chinese Academy of Sciences, Beijing 100049, China.
⁷ Department of Chemistry, School of Science, the University of Tokyo, Tokyo 113-0033, Japan.
⁸ School of Pharmacy, Hainan Medical University, Haikou 571199, China.

PMID: 38487007
PMCID: PMC10935005
DOI: 10.1016/j.apsb.2023.11.025

No abstract available

Keywords: CARTp; GPR160; Prostate cancer; Signaling pathway.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

**Figure 1**
Expression of CARTp in human prostate tissues and signal transduction induced by CARTp in cancer cell lines. (A) Images of CARTp expression in human prostate cancerous (prostatic acinar adenocarcinoma) and adjacent normal tissues detected by immunohistochemistry (IHC), scale bars, 50 μm. Black arrows in the figures indicate stained CARTp. (B, C) 41 samples containing tumor and 39 samples with tumor adjacent tissues from patients were used for IHC analysis of GPR160 (B) and CARTp (C), with unpaired t test. ∗∗∗P < 0.0001. NS, no significance. (D) Samples of 142 patients with both tumor and adjacent tissues were used for immunohistochemistry analysis of CARTp expression, with unpaired t test. NS, no significance. Data (means ± SEM) represent three independent reading. (E) Expression of CARTp and GPR160 in three cancer cell lines (differentiated PC12 cells, 22Rv1 cells and KATO III cells). D-PC12, differentiated PC12 cells. (F) Activation of the ERK1/2 phosphorylation (pERK1/2) induced by 100 μmol/L CARTp in the three cancer cell lines. Data shown are means ± SEM of at least three independent experiments, normalized with respect to baseline signal (*i.e*., vehicle treatment). D-PC12, differentiated PC12 cells. Statistical analysis was performed by one-way ANOVA followed by Dunnett's multiple comparison test. ∗∗P < 0.01.

**Figure 2**
Signaling profiles of GPR160 induced by CARTp. (A, B) CARTp-induced cAMP signaling in 22Rv1 cells and CHO-K1 cells transfected with human GPR160. Data shown are means ± SEM of three independent experiments. (C–E) Efficiency of GPR160 transfected into CHO-K1 cells using the plasmid (pCMV6-GPR160-Flag) was confirmed by immunofluorescence staining in protein level (green = GPR160-Flag, blue = nuclear staining) (C, D) and RT-qPCR (E) in mRNA level. The scale corresponds to 50 μm. Data shown are means ± SEM of three independent experiments. Statistical analysis was performed by paired t test. ∗∗P < 0.01, ∗∗∗P < 0.0001. (F) Functional analysis of the G protein couplings of GPR160 induced by CARTp. CARTp-induced dissociations of 12 heterotrimeric G proteins were measured using NanoBiT assay. Concentration-response curves were expressed as area-under-the-curve (AUC) across the time–course response curve (0–15 min) for each concentration. Data shown are means ± SEM of three independent experiments. (G, H) CARTp-induced β-arrestin1/2 recruitment. Concentration–response curves were expressed as AUC across the time–course response curve (0–15 min) for each concentration. Data shown are means ± SEM of three independent experiments.

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References

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High expression of GPR160 in prostate cancer is unrelated to CARTp-mediated signaling pathways

Affiliations

High expression of GPR160 in prostate cancer is unrelated to CARTp-mediated signaling pathways

Authors

Affiliations

Conflict of interest statement

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