ArticleOncoTargets and therapy2018
Overexpression of GPR35 confers drug resistance in NSCLC cells by β-arrestin/Akt signaling.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- GPR35 Mediates the Proliferation and Adipogenesis of Goat Intramuscular Preadipocytes Through the cAMP/PKA Signaling Pathway.Animals : an open access journal from MDPI · 2026Article
- LDCT combined with serum miR-4638-3p expression enhances NSCLC diagnostic efficacy and rs6601178 polymorphism susceptibility association.Journal of cardiothoracic surgery · 2026Article
- Role of mucosal chemokines in the development of tissue-resident CD4Frontiers in immunology · 2026Review
- Increased GPR35 expression is correlated with poor prognosis in prostate cancer.World journal of surgical oncology · 2025Article
- Review
- The power of many: Multilevel targeting of representative chemokine and metabolite GPCRs in personalized cancer therapy.European journal of immunology · 2024Review
- The chemical composition of secondary organic aerosols regulates transcriptomic and metabolomic signaling in an epithelial-endothelial in vitro coculture.Particle and fibre toxicology · 2024Article
- G protein-coupled receptors and traditional Chinese medicine: new thinks for the development of traditional Chinese medicine.Chinese medicine · 2024Review
- From orphan to oncogene: The role of GPR35 in cancer and immune modulation.Cytokine & growth factor reviews · 2024Review
- β-Arrestin2 promotes docetaxel resistance of castration-resistant prostate cancer via promoting hnRNP A1-mediated PKM2 alternative splicing.Discover oncology · 2023Article
- Pharmacohistory of Cannabis Use-A New Possibility in Future Drug Development for Gastrointestinal Diseases.International journal of molecular sciences · 2023Review
- The cryptic role of CXCL17/CXCR8 axis in the pathogenesis of cancers: a review of the latest evidence.Journal of cell communication and signaling · 2023Review
- Investigation of Flavonoid Scaffolds as DAX1 Inhibitors against Ewing Sarcoma through Pharmacoinformatic and Dynamic Simulation Studies.International journal of molecular sciences · 2023Article
- Synergies of Radiomics and Transcriptomics in Lung Cancer Diagnosis: A Pilot Study.Diagnostics (Basel, Switzerland) · 2023Article
- Involvement of CXCL17 and GPR35 in Gastric Cancer Initiation and Progression.International journal of molecular sciences · 2022Article
- GPCRs in Intracellular Compartments: New Targets for Drug Discovery.Biomolecules · 2022Review
- Article
- Review
- Therapeutic Opportunities and Challenges in Targeting the Orphan G Protein-Coupled Receptor GPR35.ACS pharmacology & translational science · 2020Review
- Prognostic value of CXCL17 and CXCR8 expression in patients with colon cancer.Oncology letters · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-small-cell lung cancer (NSCLC) is the major leading cause of cancer-related death around the world. The resistance to chemotherapy limits the effects of clinical treatment. The aim of this study was to identify novel mechanisms involved in NSCLC chemoresistance. MATERIALS AND
methodsWe explored the public database and commercial tissue microarray to evaluate the expression of G protein-coupled receptor 35 (GPR35). We established the chemoresistant A549 cell line to further investigate the biological function of GPR35 in vitro and in vivo. Then, we measured the altered signalings that GPR35 knocking down by Western blot assay.
resultsWe demonstrated that GPR35 expression was significantly elevated in NSCLC tissues and correlated with poor prognosis. GPR35 was upregulated in our in vitro chemoresistance cell model. GPR35 depletion reduced the half maximal inhibitory concentration of chemodrugs and restored the sensitivity both in vitro and in vivo. Mechanically, we found that GPR35-mediated chemoresistance occurred partially via β-arrestin-2/Akt signaling. Furthermore, inhibition of β-arrestin-2 or Akt activation could suppress the GPR35 expression and overcome chemoresistance.
conclusionOur results suggested that GPR35 might serve as a novel therapeutic target to enhance the chemotherapy efficacy in NSCLC.
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