LPAR3 (Lysophosphatidic Acid Receptor 3)

These results suggest that, compared to parental MG-63 cells, highly migratory osteosarcoma MG63-R10 cells adapt their malignant cellular functions to hypoxic and low-glucose conditions through LPA receptor signaling, highlighting this pathway as a potential therapeutic target in aggressive osteosarcomas. The online version contains supplementary material available at 10.1007/s12195-025-00873-y.

CoCl2 also increased AGS cell viability in response to cisplatin (CDDP) in the presence of LPA...Our results demonstrate that LPA receptor signaling is differentially regulated under CoCl2-induced and true hypoxia, contributing to distinct outcomes in cell motility and drug response. This suggests that LPA receptor signaling is a potential target for controlling hypoxia-induced malignant transformation in gastric cancer cells.

Nonetheless, further experimental validation and extensive clinical research are necessary to enable the application of these findings in clinical practice. These results highlight the potential of targeting glycolytic pathways as a promising approach to improve the management and treatment outcomes of OC.

In the presence of LPA, cell viability to cisplatin (CDDP) was higher in A549-R12 cells cultured at both 21 % and 1 % O2 compared to A549 cells. These results suggest that LPA receptor signaling plays a key role in regulating malignant progression in highly migratory lung cancer cells under hypoxic conditions.

These results indicate that the inhibition of LPA receptor signaling by metformin, especially the consequent suppression of LPAR3-mediated cell migration, may contribute to the antitumor effects of metformin.

Based on the investigation, we confirmed that matrix stiffness governs the progression of nasopharyngeal carcinoma and that LPAR3 and COL8A1, as matrix stiffness related biomarkers, promote nasopharyngeal carcinoma metastasis by inducing epithelial-mesenchymal transition and angiogenesis. Overall, the in-depth exploration of matrix stiffness may provide a strategy for clinical treatment intervention and provide promising targets for clinical nasopharyngeal carcinoma treatment.

Additionally, the viability of AGS cells in response to cisplatin (CDDP) was enhanced under low glucose, low glutamine, and low amino acid conditions. The motility and viability of AGS cells in response to CDDP were significantly increased by AM966 (LPA1 antagonist), GRI-977143 (LPA2 agonist) and (2S)-OMPT (LPA3 agonist). These results suggest that LPA receptor signaling is significantly implicated in regulating malignant properties in AGS cells under low nutrient conditions.

LPAR2 and PLPP2 inhibition are also predicted to have potential therapeutic utility. Future multi-omics investigations are necessarily to validate which LPA signaling components are high-value candidates for pharmacological manipulation in PDAC treatment.

Our prognostic model elaborates on the roles of GPCRRGs in OV and provides a new tool for prognosis and immune response prediction in patients with OV.

These results suggest that LPA receptor-mediated signaling plays an important role in the acquisition of malignant properties in long-term TAM treated MCF-7 cells under hypoxic and estrogen-deprived conditions.

Furthermore, the tube formation of SVEC4-10 cells was increased by AM966. These results suggest that LPA receptor-mediated signaling contributes to the modulation of hypoxic-induced biological functions of lymphatic endothelial cells.

In cell survival assay, (2 S)-OMPT suppressed the cell survival to cisplatin (CDDP) of MG-63 cells irradiated with X-rays (8 Gy)...The cell survival to CDDP of X-ray irradiated cells was increased by LPA2 agonist GRI-977143 and reduced by LPA2 knockdown. These results suggest that LPA receptor-signaling participates in the modulation of cellular functions induced by X-ray irradiation in osteosarcoma cells.