---
title: "GPR68 Drives TNBC Progression and Cuproptosis Resistance via MEK/ERK Signaling"
id: "pubmed-42776031"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42776031"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42776031/"
doi: "10.1096/fj.202600988R"
published_at: "2026-09-30T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# GPR68 Drives TNBC Progression and Cuproptosis Resistance via MEK/ERK Signaling
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42776031
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42776031/)
- **DOI:** [10.1096/fj.202600988R](https://doi.org/10.1096%2Ffj.202600988R)
- **Published At:** 2026-09-30T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The study identified **GPR68** (G protein-coupled receptor 68) as a gene associated with **cuproptosis** that is highly expressed in triple-negative breast cancer (**TNBC**) using weighted gene co-expression network analysis (WGCNA) on TNBC gene expression data. - Experimental knockdown of **GPR68** reduced TNBC cell proliferation, migration, and invasion, indicating a pro-tumorigenic role in vitro. - Loss of **GPR68** increased sensitivity of TNBC cells to cuproptosis when exposed to copper ionophore ES-Cu, producing cellular copper accumulation; this increased cell death was reversed by the copper chelator tetrathiomolybdate (TTM). - Correlation analyses showed that **GPR68** regulates expression of glutaminase (**GLS**); knockdown of **GLS** abrogated the pro-growth effects of **GPR68** and restored cuproptosis susceptibility. - Pathway enrichment implicated the mitogen-activated protein kinase (**MAPK**) pathway; **GPR68** overexpression elevated ERK phosphorylation, linking to the **MEK/ERK** axis. - Pharmacologic blockade of ERK signaling with **Trametinib** inhibited the effects of **GPR68** on TNBC progression and on cuproptosis resistance, indicating MEK/ERK dependence. - Overall, the data suggest **GPR68** promotes TNBC development and confers resistance to cuproptosis through a **GLS–MEK/ERK** regulatory network, highlighting **GPR68** and related nodes as potential targets for cuproptosis-based TNBC therapies. - The report provides mechanistic insight but full experimental details, sample sizes, in vivo data, and specific quantitative results were not included in the PubMed abstract and therefore are not reported here.
## Clinical Analysis & Structured Key Points
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more resources ](https://pubmed.ncbi.nlm.nih.gov/42776031/#linkout) Title & authors Abstract Similar articles References MeSH terms Substances Related information Grants and funding LinkOut - more resources FASEB J Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22FASEB+J%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22FASEB+J%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42776031/) . 2026 Sep 30;40(18):e72312. doi: 10.1096/fj.202600988R. # G Protein-Coupled Receptor 68 Promotes the Progression of Triple-Negative Breast Cancer and Cuproptosis Resistance via the MEK/ERK Signaling Pathway [Jia Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+J&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-2 "Henan Provincial Engineering Research Center of Transformation and Application of Traditional Chinese and Western Medicine for Malignant Tumor, Zhengzhou, China."), [Shilei Gao](https://pubmed.ncbi.nlm.nih.gov/?term=Gao+S&cauthor_id=42776031)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-3 "Department of Bone and Soft Tissue, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Lihan Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+L&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Lu Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+L&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Xu Sun](https://pubmed.ncbi.nlm.nih.gov/?term=Sun+X&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Huahua Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+H&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Bian Shi](https://pubmed.ncbi.nlm.nih.gov/?term=Shi+B&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Huaimin Liu](https://pubmed.ncbi.nlm.nih.gov/?term=Liu+H&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#full-view-affiliation-2 "Henan Provincial Engineering Research Center of Transformation and Application of Traditional Chinese and Western Medicine for Malignant Tumor, Zhengzhou, China.") Affiliations Expand ### Affiliations * 1 Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China. * 2 Henan Provincial Engineering Research Center of Transformation and Application of Traditional Chinese and Western Medicine for Malignant Tumor, Zhengzhou, China. * 3 Department of Bone and Soft Tissue, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China. * PMID: **42776031** * DOI: [ 10.1096/fj.202600988R ](https://doi.org/10.1096/fj.202600988r) Item in Clipboard # G Protein-Coupled Receptor 68 Promotes the Progression of Triple-Negative Breast Cancer and Cuproptosis Resistance via the MEK/ERK Signaling Pathway Jia Wang et al. FASEB J. 2026. Show details Display options Display options Format Abstract PubMed PMID FASEB J Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22FASEB+J%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22FASEB+J%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42776031/) . 2026 Sep 30;40(18):e72312. doi: 10.1096/fj.202600988R. ### Authors [Jia Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+J&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-2 "Henan Provincial Engineering Research Center of Transformation and Application of Traditional Chinese and Western Medicine for Malignant Tumor, Zhengzhou, China."), [Shilei Gao](https://pubmed.ncbi.nlm.nih.gov/?term=Gao+S&cauthor_id=42776031)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-3 "Department of Bone and Soft Tissue, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Lihan Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+L&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Lu Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+L&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Xu Sun](https://pubmed.ncbi.nlm.nih.gov/?term=Sun+X&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Huahua Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+H&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Bian Shi](https://pubmed.ncbi.nlm.nih.gov/?term=Shi+B&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China."), [Huaimin Liu](https://pubmed.ncbi.nlm.nih.gov/?term=Liu+H&cauthor_id=42776031)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-1 "Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42776031/#short-view-affiliation-2 "Henan Provincial Engineering Research Center of Transformation and Application of Traditional Chinese and Western Medicine for Malignant Tumor, Zhengzhou, China.") ### Affiliations * 1 Department of Integrated Traditional Chinese and Western Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China. * 2 Henan Provincial Engineering Research Center of Transformation and Application of Traditional Chinese and Western Medicine for Malignant Tumor, Zhengzhou, China. * 3 Department of Bone and Soft Tissue, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China. * PMID: **42776031** * DOI: [ 10.1096/fj.202600988R ](https://doi.org/10.1096/fj.202600988r) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID Linked Discoveries ## Abstract Cuproptosis is a type of cell death that depends on the energy production process inside cells, and it is important in cancer treatment. This study aimed to identify cuproptosis-associated genes in triple-negative breast cancer (TNBC) and reveal regulatory pathways. We applied weighted gene co-expression network analysis to screen gene expression data from TNBC patients. Cuproptosis-associated genes were identified at the intersection of the co-expression modules and the cuproptosis gene dataset. G protein-coupled receptor 68 (GPR68) was identified as a cuproptosis-associated gene that is highly expressed in TNBC cells. Knockdown of GPR68 inhibited TNBC cell growth, migration, and invasion. The knockdown of GPR68 enhanced cuproptosis in TNBC cells when stimulated with ES-Cu, leading to an accumulation of cellular copper. This effect was reversed by the copper chelator tetrathiomolybdate. Correlation analysis verified that GPR68 regulates glutaminase (GLS) expression in TNBC cells. GLS knockdown reversed the promoted role of GPR68 in TNBC progression and the inhibitory role of GPR68 in TNBC cell cuproptosis. We further investigated the role of GPR68 in TNBC through pathway enrichment analysis, which revealed significant enrichment in the mitogen-activated protein kinase (MAPK) signaling pathway. GPR68 overexpression increased the levels of ERK phosphorylation. The ERK signaling pathway inhibitor, Trametinib, blocked the effects of GPR68 on TNBC progression and cuproptosis. GPR68 knockdown hindered TNBC development and induced cell cuproptosis by regulating the MEK/ERK signaling pathway, which is linked to GLS. This study provides new insights into developing cuproptosis targets for TNBC treatment. **Keywords:** G protein‐coupled receptor 68; MEK/ERK signaling pathway; cuproptosis; glutaminase; triple‐negative breast cancer. © 2026 Federation of American Societies for Experimental Biology. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Similar articles * [ PRKCQ promotes oncogenic growth and anoikis resistance of a subset of triple-negative breast cancer cells. ](https://pubmed.ncbi.nlm.nih.gov/27663795/) Byerly J, Halstead-Nussloch G, Ito K, Katsyv I, Irie HY.Byerly J, et al.Breast Cancer Res. 2016 Sep 23;18(1):95. doi: 10.1186/s13058-016-0749-6.Breast Cancer Res. 2016.PMID: 27663795Free PMC article. * [ Knocking Down Ferredoxin 1 Inhibits the Progression of Colorectal Cancer and Regulates Cuproptosis via Mediating the Hippo Signaling Pathway. ](https://pubmed.ncbi.nlm.nih.gov/39987563/) Hu Y, Liu H, Tan X, Wu X.Hu Y, et al.Mol Carcinog. 2025 May;64(5):911-922. doi: 10.1002/mc.23897. Epub 2025 Feb 23.Mol Carcinog. 2025.PMID: 39987563 * [ SNHG14 promotes triple-negative breast cancer cell proliferation, invasion, and chemoresistance by regulating the ERK/MAPK signaling pathway. ](https://pubmed.ncbi.nlm.nih.gov/39266460/) Wang B, Xing AY, Li GX, Liu L, Xing C.Wang B, et al.IUBMB Life. 2024 Dec;76(12):1295-1308. doi: 10.1002/iub.2910. Epub 2024 Sep 12.IUBMB Life. 2024.PMID: 39266460 * [ GPER mediates enhanced cell viability and motility via non-genomic signaling induced by 17β-estradiol in triple-negative breast cancer cells. ](https://pubmed.ncbi.nlm.nih.gov/24874276/) Yu T, Liu M, Luo H, Wu C, Tang X, Tang S, Hu P, Yan Y, Wang Z, Tu G.Yu T, et al.J Steroid Biochem Mol Biol. 2014 Sep;143:392-403. doi: 10.1016/j.jsbmb.2014.05.003. Epub 2014 May 27.J Steroid Biochem Mol Biol. 2014.PMID: 24874276 * [ ZMIZ2/MCM3 Axis Participates in Triple-Negative Breast Cancer Progression. ](https://pubmed.ncbi.nlm.nih.gov/41502508/) Zou X, Sun M, Jiang X, Yu J, Li X, Nie B.Zou X, et al.Oncol Res. 2025 Dec 30;34(1):15. doi: 10.32604/or.2025.066662. eCollection 2025.Oncol Res. 2025.PMID: 41502508Free PMC article. [ See all similar articles ](https://pubmed.ncbi.nlm.nih.gov/?linkname=pubmed_pubmed&from_uid=42776031) ## References 1. 1. S. K. Yeo and J. L. Guan, “Breast Cancer: Multiple Subtypes Within a Tumor?,” Trends Cancer 3 (2017): 753–760. 2. 1. F. Borri and A. Granaglia, “Pathology of Triple Negative Breast Cancer,” Seminars in Cancer Biology 72 (2021): 136–145. 3. 1. X. Li, J. Yang, L. Peng, et al., “Triple‐Negative Breast Cancer Has Worse Overall Survival and Cause‐Specific Survival Than Non‐Triple‐Negative Breast Cancer,” Breast Cancer Research and Treatment 161 (2017): 279–287. 4. 1. Y. Liu, J. He, J. Chen, et al., “Programmed Cell Death in Triple‐Negative Breast Cancer,” Cellular & Molecular Biology Letters 30 (2025): 111. 5. 1. F. Peng, M. Liao, R. Qin, et al., “Regulated Cell Death (RCD) in Cancer: Key Pathways and Targeted Therapies,” Signal Transduction and Targeted Therapy 7 (2022): 286. Show all 37 references ## MeSH terms * Cell Line, Tumor Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Line%2C+Tumor%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Line%2C+Tumor) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42776031/) * Cell Movement Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Movement%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](htt
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