ArticleJournal of clinical biochemistry and nutrition2023
GPRC5A regulates proliferation and oxidative stress by inhibiting the STAT3/Socs3/c-MYC pathway in hepatocellular carcinoma.
Article in Journal of clinical biochemistry and nutrition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Multi-omics characterization of a GPRC5AJournal of translational medicine · 2026Article
- Targeting NETO2 suppresses cell proliferation, invasion, and migration and inactivates the STAT3/C-MYC pathway in hepatocellular carcinoma.World journal of surgical oncology · 2025Article
- Expression of signal recognition particle 14 in hepatocellular carcinoma and its relationship with disease progression and patient survival.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Article
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Authors and funding
4 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The G protein-coupled receptor, class C, group 5, member A (GPRC5A) plays a key role in various diseases, but its effect on hepatocellular carcinoma (HCC) and the potential underlying mechanisms remains unclear. In the present study, we explored the effect of GPRC5A on the progression of HCC and further explored its mechanism of action. The results revealed that the expression of GPRC5A was lower in HCC tissues and cells. Overexpression of GPRC5A suppressed the proliferation and epithelial-mesenchymal transition (EMT) of HCC cells. In addition, overexpression of GPRC5A induced oxidative stress and apoptosis. Further study showed that overexpression of GPRC5A inhibited the expression of STAT3/Socs3/c-MYC related-protein and the NLRP3 inflammasome. Moreover, the STAT3/Socs3/c-MYC and NLRP3 inflammasome was involved in the effect of GPRC5A on HCC cells. These results suggest that GPRC5A suppresses proliferation and EMT, induces oxidative stress and leads to apoptosis of HCC cells, potentially by regulating STAT3/Socs3/c-MYC signalling and the NLRP3 inflammasome. These findings suggest that GPRC5A has an anti-tumor effect in the formation of HCC, and the molecular therapy of GPRC5A provides a theoretical basis for treating HCC.
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