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Molecular and Cellular Research on Taste Receptors

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 1577

Special Issue Editor


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Guest Editor
RISE-Health, UBI—Department of Medical Sciences, Faculty of Health Sciences, University of Beira Interior, Covilhã, Portugal
Interests: taste receptors; glioblastoma; cancer; bitter taste; sweet taste

Special Issue Information

Dear Colleagues,

The gustatory system plays a central role in food perception, nutrition, and overall health, while also contributing to metabolic regulation and disease processes. Recent advances in molecular and cellular research have provided remarkable insights into the mechanisms underlying taste perception, from receptor biology and signal transduction to cellular interactions and functional roles in pathological contexts. This Special Issue aims to highlight cutting-edge research in the molecular and cellular biology of taste receptors in health and disease. We welcome original research articles and reviews exploring the molecular and cellular mechanisms of taste receptor signaling, their expression and regulation in normal and pathological contexts, and their functional roles in health and disease, including cancer. Studies investigating how taste receptors influence cellular behavior, tissue function, or disease-related processes are encouraged. Experimental, translational, and computational approaches that elucidate receptor mechanisms or potential therapeutic applications are particularly encouraged. This Special Issue seeks to provide a comprehensive understanding of taste receptor biology beyond gustatory perception, fostering novel insights of its relevance to health and disease.

Dr. Ana R. Costa
Guest Editor

Manuscript Submission Information

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Keywords

  • taste receptors
  • taste signaling
  • gustatory system
  • molecular signaling
  • cellular mechanisms
  • health and disease
  • functional roles
  • neurobiology of taste
  • cancer biology and metastasis
  • translational research

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Published Papers (2 papers)

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Research

16 pages, 2216 KB  
Article
Bitter Taste Signalling via TAS2R43 Enhances Temozolomide Efficacy in Glioblastoma Cells
by Ana R. Costa, Ana C. Duarte, Isabel Gonçalves, Robert Preissner, José F. Cascalheira, Helena Marcelino and Cecília R. A. Santos
Int. J. Mol. Sci. 2026, 27(7), 3262; https://doi.org/10.3390/ijms27073262 - 3 Apr 2026
Viewed by 661
Abstract
Bitter taste receptors (TAS2Rs) are increasingly recognised as extraoral chemosensors that modulate diverse biological processes, including cancer cell behaviour and drug responsiveness. Many TAS2R ligands correspond to therapeutic compounds; however, their contribution to the response of brain tumours to chemotherapy remains unexplored. Here, [...] Read more.
Bitter taste receptors (TAS2Rs) are increasingly recognised as extraoral chemosensors that modulate diverse biological processes, including cancer cell behaviour and drug responsiveness. Many TAS2R ligands correspond to therapeutic compounds; however, their contribution to the response of brain tumours to chemotherapy remains unexplored. Here, we investigated whether the bitter taste signalling pathway is modulated by temozolomide (TMZ), the standard chemotherapeutic agent for glioblastoma, with an impact on treatment efficacy in glioblastoma cells. We show that TMZ elicits intracellular Ca2+ responses compatible with activation of G-protein-coupled receptor signalling and induces anti-proliferative and pro-apoptotic effects in multiple human glioblastoma cell lines. Pharmacological inhibition of bitter taste receptors, as well as genetic silencing of the taste transduction G protein GNAT3, significantly attenuated TMZ-induced cytotoxicity, suggesting that bitter taste signalling is involved in this process. In silico ligand prediction combined with receptor expression profiling identified TAS2R43 as a candidate modulator of these effects, and TAS2R43 knockdown markedly reduced TMZ-induced loss of cell viability and apoptosis. Moreover, TMZ enhanced intracellular accumulation of the ABC transporter substrate doxorubicin, suggesting modulation of multidrug efflux mechanisms. Collectively, our findings identify TAS2R43 as a potential biomarker that warrants further validation to improve responses to TMZ and other ABC transporter-limited anticancer drugs. Full article
(This article belongs to the Special Issue Molecular and Cellular Research on Taste Receptors)
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29 pages, 5835 KB  
Article
Bile Canalicular Bitter Taste Receptors Inhibit β-Adrenergic Receptor-Induced Lipolysis in Steatotic Hepatocytes
by Yan-Bo Xue, Shi-Meng Gong, Yuan-Yuan Peng, Defu Yu, Ruhong Zhou and Liquan Huang
Int. J. Mol. Sci. 2026, 27(7), 3226; https://doi.org/10.3390/ijms27073226 - 2 Apr 2026
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Abstract
Bitter taste receptors (TAS2Rs) are G protein-coupled receptors best known for detecting bitter compounds in the oral cavity. However, their expression patterns and physiological roles in the liver remain largely unexplored. Here, we employed molecular and immunohistochemical approaches to demonstrate that multiple TAS2Rs [...] Read more.
Bitter taste receptors (TAS2Rs) are G protein-coupled receptors best known for detecting bitter compounds in the oral cavity. However, their expression patterns and physiological roles in the liver remain largely unexplored. Here, we employed molecular and immunohistochemical approaches to demonstrate that multiple TAS2Rs are expressed in human Hep3B cells and mouse primary hepatocytes (MPHs) and co-localized with β-adrenergic receptors (βARs) at the bile canaliculi. Bioluminescence resonance energy transfer (BRET), cAMP assays, and Western blot analyses revealed that certain TAS2Rs exhibit ligand-dependent coupling preferences for the G protein subunits Gαi1, Gαi2, and Gαi3. This coupling leads to inhibition of cAMP production and a reduction in protein kinase A (PKA) substrate phosphorylation. Biochemical assays further showed that TAS2R activation significantly attenuates βAR-mediated lipolysis, as well as the production of glycerol and free fatty acid in both Hep3B cells and MPHs. These effects were partially reversed by small interfering RNA (siRNA)-mediated knockdown of TAS2Rs. Moreover, studies using a steatotic mouse model demonstrated that bitter compounds inhibit lipid droplet degradation, resulting in hepatic triacylglycerol accumulation. Collectively, these findings reveal a role for TAS2Rs in modulating hepatic lipid metabolism and highlight their potential as therapeutic targets for the prevention and treatment of liver diseases. Full article
(This article belongs to the Special Issue Molecular and Cellular Research on Taste Receptors)
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