Background Previous reports showed that APOC1 was associated with several cancers but the function of APOC1 in cervical cancer was unknown. This study aimed to investigate the clinical effect and function of APOC1 in cervical cancer. Materials and Methods In this study, the relative expression of APOC1 in cervical cancer was detected by RT-qPCR. In order to determine the cell proliferation and migration and invading ability and apoptosis more accurately, we used CCK8 assay, Edu assay, wound healing assay, migration and invasion assay, flow cytometry assay, co-immunoprecipitation, proteomics and Western blot by silencing and overexpressing APOC1 , respectively. The role of APOC1 on tumor progression was explored in vitro and vivo. Results The relative expression of APOC1 in cervical cancer tissues was up-regulated (P<0.05). In cervical cancer cell lines, silencing of APOC1 restrained cell progression and EMT, while over-expression of APOC1 accelerated cell progression and EMT in vivo and vitro (P<0.05). Conclusion APOC1 acts as an oncogene in cervical cancers and knockdown of APOC1 inhibited cervical cancer cells growth in vitro and in vivo. There is a close relationship between the relative expression of APOC1 and clinical outcome in cervical cancer patients.

The aim of the present study was to analyze the expression of WW-domain oxidoreductase (WWOX), fragile histidine triad (FHIT) and p73 in acute lymphoblastic leukemia (ALL). Samples from 122 ALL patients and 35 non-ALL control patients were collected in this study. RT-PCR was performed to detect the mRNA expression of WWOX, FHIT and p73. The methylation status of the WWOX promoter region, FHIT promoter region and the first exon region of p73 were also analyzed using the methylation-specific PCR method. The mRNA expression of WWOX, FHIT and p73 was significantly lower in the ALL samples compared with the controls (48.2, 42.9 and 55.4%, respectively). By contrast, the methylation frequency of WWOX, FHIT and p73 was significantly higher in the ALL samples compared with the controls (44.6, 46.4 and 37.5%, respectively). The mRNA expression of these three genes was inversely correlated with the methylation frequency in the ALL samples (correlation coefficients, −0.661, −0.685 and −0.536 for WWOX, FHIT and p73, respectively). Moreover, the mRNA expression of WWOX was positively correlated with that of FHIT and p73 (correlation coefficients, 0.569 and 0.556, respectively). However, the methylation status of WWOX had no correlation with that of FHIT or p73. It was concluded that the high methylation status of WWOX, FHIT and p73 may lead to the inactivation of expression and the silencing of these genes, promoting the occurrence and development of ALL. The determination of the mRNA expression and methylation status of WWOX, FHIT and p73 may aid in the development of treatment approaches for ALL.

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