Influence of -Regulated Expression on Lung Adenocarcinoma Proliferation

Objective Aberrant expression of ATP binding cassette subfamily B member 1 () plays a key role in several cancers. However, influence of G protein coupled receptor family C group 5 type A (GPRC5A)-regulated expression on lung adenocarcinoma proliferation remains unclear. Therefore, this study investigated the effect of regulated expression on the proliferation of lung adenocarcinoma. Methods expressions in lung adenocarcinoma cell lines, human lung adenocarcinoma tissues, and tracheal epithelial cells and lung tissues of knockout mice and wild-type mice were analyzed with RT-PCR, Western blot, or immunohistochemical analysis. Cell counting kit-8 assay was performed to analyze the sensitivity of tracheal epithelial cells from knockout mice to chemotherapeutic agents. Subcutaneous tumor formation assay was performed to confirm whether down-regulation of could inhibit the proliferation of lung adenocarcinoma . To verify the potential regulatory relationship between GPRC5A and ABCB1, immunofluorescence and immunoprecipitation assays were performed. Results ABCB1 expression was up-regulated in lung adenocarcinoma cell lines and human lung adenocarcinoma tissues. ABCB1 expression in the tracheal epithelial cells and lung tissues of deficient mice was higher than that in the wild type mice. Tracheal epithelial cells of knockout mice were much more sensitive to tariquidar and doxorubicin than those of wild type mice. Accordingly, 28 days after injection of the transplanted cells, the volume and weight of lung tumor in knockout cell-transplanted GPRC5AC57BL/6 mice were significantly smaller than those in wild type cell-transplanted mice (= 0.0043, = 0.0060). Furthermore, immunofluorescence and immunoprecipitation assays showed that GPRC5A regulated ABCB1 expression by direct binding.Conclusion GPRC5A reduces lung adenocarcinoma proliferation inhibiting expression. The pathway by which GPRC5A regulates expression needs to be investigated.