RESUMEN
This study aimed to investigate the roles of PALMD in ovarian cancer. mRNA expression was detected using RT-qPCR. The aldehyde dehydrogenase (ALDH) activity and biomarkers of ovarian cancer stem cells were determined using flow cytometry. The stemness of ovarian cancer cells was determined using sphere formation assay. Cell viability was determined using CCK-8 assay. The number of colonies was determined using colony formation assay. Cell migration was detected using wound healing assay. Cell invasion was determined using transwell assay. The results showed that PALMD was downregulated in ovarian cancer. Overexpressed PALMD inhibited the proliferative, migrative, and invasive ability of ovarian cancer cells. Moreover, PALMD inhibited the stem-like properties of ovarian cancer cells. Additionally, PALMD downregulated ring finger protein 145 (RNF145) expression, overexpression of which contributed to the aggressiveness of ovarian cancer cells. Taken together, PALMD suppressed ovarian cancer cell stem specification via inhibiting RNF145 expression.
Asunto(s)
Movimiento Celular , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Células Madre Neoplásicas , Neoplasias Ováricas , Humanos , Femenino , Neoplasias Ováricas/genética , Neoplasias Ováricas/metabolismo , Neoplasias Ováricas/patología , Células Madre Neoplásicas/metabolismo , Línea Celular Tumoral , Ubiquitina-Proteína Ligasas/metabolismo , Ubiquitina-Proteína Ligasas/genética , Regulación hacia AbajoRESUMEN
HDAC1 functions as an oncogene in multi-type cancers. This study aimed to investigate the roles of histone deacetylase 1 (HDAC1) in cervical cancer (CC). mRNA expression was determined using reverse transcription quantitative polymerase chain reaction. The protein-protein complexes was analyzed using co-immunoprecipitation assay. The binding sites between NRF2 and NEU1 were confirmed by chromatin immunoprecipitation assay. Cell viability was detected by CCK-8. Cell proliferation was measured using CCK-8 and colony formation assays. Cell migrative and invasive ability were determined using transwell assay. We found that HDAC1 was upregulated in CC patients and cells. Trichostatin A (TSA) treatment decreased the number of colonies and migrated and invaded cells. Moreover, HDAC1 interacted with NRF2 to downregulate NEU1 expression. NEU1 knockdown attenuated the effects of TSA and enhanced the aggressiveness of CC cells. In conclusion, HDAC1 functions as an oncogene in CC. Targeting HDAC1 may be an alternative strategy for CC.