RESUMEN
BACKGROUND: The centromere protein O (CENPO) is an important member of the centromere protein family. However, the role of CENPO in pan-cancer and immune infiltration has not been reported. Here, we investigated the role of CENPO in pan-cancer and further validated its role in lung adenocarcinoma (LUAD) by in vitro experiments. METHOD: The UCSC Xena database and The Cancer Genome Atlas (TCGA)-LUAD data were used to assess the expression levels of CENPO. The potential value of CENPO as a diagnostic and prognostic biomarker for pan-cancer was evaluated using TCGA data and the GEPIA database. The -expression profiles of LUAD patients and the corresponding clinical data were downloaded for correlation analysis. The role of CENPO in immune infiltration was investigated using the UCSC Xena database. Subsequently, qRT-PCR was performed to detect the expression of CENPO. Cell proliferation, migration, and invasion were determined using CCK-8, wound-healing assay, and transwell assay, respectively. RESULTS: CENPO is highly expressed in most cancers, and the upregulation of CENPO is associated with poor prognosis in many cancers. CENPO expression correlates with age, TNM stage, N stage, T stage, and receipt of radiotherapy in LUAD patients, and LUAD patients with high CENPO expression have poorer overall survival (OS) and disease-free survival (DFS). In addition, CENPO expression is associated with immune cell infiltration and immune checkpoint inhibitors. Moreover, the expression of CENPO was closely related to the expression of tumor mutational load and microsatellite instability. In vitro experiments showed that CENPO expression was increased in LUAD cell lines and that knockdown of CENPO significantly inhibited the proliferation, cell invasion, and migration ability of LUAD cells. CONCLUSION: CENPO may be a potential pan-cancer biomarker and oncogene, especially in LUAD. In addition, CENPO is associated with immune cell infiltration and may serve as a new molecular therapeutic target and effective prognostic marker for LUAD.
Asunto(s)
Adenocarcinoma del Pulmón , Proteínas Cromosómicas no Histona , Neoplasias Pulmonares , Humanos , Adenocarcinoma del Pulmón/genética , Biomarcadores de Tumor/genética , Proliferación Celular/genética , Proteínas Cromosómicas no Histona/genética , Neoplasias Pulmonares/genética , PronósticoRESUMEN
Hepatocellular carcinoma (HCC) is a major global public health concern, with approximately 79 million new cases and 75 million HCC-related deaths occurring annually worldwide. Among the drugs, cisplatin (DDP) is considered a cornerstone and has been shown to significantly inhibit cancer progression. However, the mechanism underlying DDP-resistance in HCC remains unclear. This study aimed to identify a novel lncRNA. FAM13A Antisense RNA 1 (FAM13A-AS1), that promotes the proliferation of DDP-resistant HCC cells and to elucidate its downstream and upstream mechanisms in the progression of HCC DDP-resistance. Our results suggest that FAM13A-AS1 interacts directly with Peroxisome Proliferator Activated Receptor γ (PPARγ), stabilizing its protein through de-ubiquitination. Moreover, our findings indicate that Paired Like Homeobox 2B (PHOX2B) transcriptionally regulates the expression of FAM13A-AS1 in HCC cells. These results shed new light on the understanding of the progression of HCC DDP-resistance.