Drareg
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- Feb 18, 2016
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Abstract
OBJECTIVE:
Non-small cell lung cancer (NSCLC) is the most common type of human lung cancer leading cause of cancer death worldwide. However, first-line drugs such as gefitinib and erlotinib showed great drug resistance in the clinical.
MATERIALS AND METHODS:
The cell proliferation was evaluated by MTT assay; gene expression was detected by qPCR assay. The protein expression was analyzed by Western blotting.
RESULTS:
Our results showed that in mouse models of lung cancer by A549 or NCI-H1975 xenograft, the local anesthetic drug Procaine (PCA) with 50 mg/kg specifically attenuated tumors compared with the vehicle-treated group. In vitro, PCA suppressed both two human NSCLC cell lines A549 and NCI-H1975 proliferation in a lower dose (at nM grade). The cell proliferation marker PCNA was also downregulated after PCA treatment in vivo. Furthermore, low-dose of PCA could inhibit the mRNA expression of the key NSCLC target EGFR selectively in the A549 cells, however, it was not observed in another cell line NCI-H1975, implying a specific signaling by PCA in the cell type.
CONCLUSIONS:
Taken together, our data indicate that PCA treatment leads to suppression of tumor growth and proliferation in A549 and NCI-H1975, and there is an EGFR transcription pathway by PCA in A549 cells.
The effect of low dosage of procaine on lung cancer cell proliferation. - PubMed - NCBI
OBJECTIVE:
Non-small cell lung cancer (NSCLC) is the most common type of human lung cancer leading cause of cancer death worldwide. However, first-line drugs such as gefitinib and erlotinib showed great drug resistance in the clinical.
MATERIALS AND METHODS:
The cell proliferation was evaluated by MTT assay; gene expression was detected by qPCR assay. The protein expression was analyzed by Western blotting.
RESULTS:
Our results showed that in mouse models of lung cancer by A549 or NCI-H1975 xenograft, the local anesthetic drug Procaine (PCA) with 50 mg/kg specifically attenuated tumors compared with the vehicle-treated group. In vitro, PCA suppressed both two human NSCLC cell lines A549 and NCI-H1975 proliferation in a lower dose (at nM grade). The cell proliferation marker PCNA was also downregulated after PCA treatment in vivo. Furthermore, low-dose of PCA could inhibit the mRNA expression of the key NSCLC target EGFR selectively in the A549 cells, however, it was not observed in another cell line NCI-H1975, implying a specific signaling by PCA in the cell type.
CONCLUSIONS:
Taken together, our data indicate that PCA treatment leads to suppression of tumor growth and proliferation in A549 and NCI-H1975, and there is an EGFR transcription pathway by PCA in A549 cells.
The effect of low dosage of procaine on lung cancer cell proliferation. - PubMed - NCBI
