RESUMO
Multiple studies have shown that CC motif chemokine ligand 19 (CCL19) promotes cell proliferation in several human cancers. The aim of this study was to investigate the expression and function of CCL19 in hepatocellular carcinoma (HCC). Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blot, and immunohistochemistry were performed separately to detect the expression of CCL19 in HCC tissues. The expression of CCL19 and its receptor (CCR7) in different HCC cell lines were screened by Western blot. HCC cell lines were screened and processed with recombinant human CCL19 (rhCCL19) or si-CCL19 RNA. Cell proliferation assay and transwell assay were performed to evaluate the proliferation and migration of HCC cells, respectively. Low expression of CCL19 was observed in 83.72 % (72/86) of the HCC versus 16.67 % (4/24) of the adjacent non-tumorous liver tissues, the difference of CCL19 expression between HCC and adjacent non-tumorous liver tissues was statistically significant (P < 0.001). The expression level of CCL19 mRNA and protein in tumor tissues was significantly lower than adjacent non-tumorous liver tissues. The proliferation and migration of HCC cells were obviously inhibited in rhCCL19-treated groups. Our data suggest that CCL19 may play a suppressive role in the regulation of aggressiveness in human HCC.
Assuntos
Carcinoma Hepatocelular/metabolismo , Quimiocina CCL19/metabolismo , Neoplasias Hepáticas/metabolismo , Adulto , Idoso , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Carcinoma Hepatocelular/cirurgia , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Movimento Celular/genética , Proliferação de Células/efeitos dos fármacos , Quimiocina CCL19/genética , Quimiocina CCL19/farmacologia , Feminino , Expressão Gênica , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/cirurgia , Masculino , Pessoa de Meia-Idade , Gradação de Tumores , Interferência de RNA , RNA Interferente Pequeno/genética , Carga TumoralRESUMO
Polymorphisms in DNA repair genes have been shown to influence DNA repair processes and to modify cancer susceptibility. Here we conducted a case-control study to assess the role of potential SNPs of DNA repair genes on the risk of glioma and meningioma. We included 297 cases and 458 cancer-free controls. Genotyping of XRCC1 Gln399Arg, XRCC1 Arg194Trp, XRCC2 Arg188His, XRCC3 Thr241Met, XRCC4 Ala247Ser, ERCC1 Asn118Asp, ERCC2 Lys751Gln and ERCC5 Asp1558His were performed in a 384-well plate format on the Sequenom MassARRAY platform. XRCC1 Arg194Trp (rs1799782) and ERCC2 Asp312Asn rs1799793 did not follow the HWE in control group, and genotype distributions of XRCC1 Gln399Arg rs25487, XRCC2 Arg188His rs3218536 and ERCC2 Asp312Asn rs1799793 were significantly different between cases and controls (P<0.05). We found XRCC1 399G/G, XRCC1 194 T/T and XRCC3 241T/T were associated with a higher risk when compared with the wild-type genotype. For ERCC5 Asp1558His, we found G/G genotype was associated with elevated susceptibility. In conclusion, our study has shown that XRCC1 Gln399Arg, XRCC1 Arg194Trp, XRCC3 Thr241Met and ERCC5 Asp1558His are associated with risk of gliomas and meningiomas. This finding could be useful in identifying the susceptibility genes for these cancers.
