RAN binding protein 9 (RANBP9) is widely expressed in mammalian tissues, including osteosarcoma, lung, gastric and breast cancer tissues. However, currently, not much is known about the role of RANBP9 in colorectal cancer (CRC). In the present study, RANBP9 expression in CRC tissues and cell lines was measured by immunohistochemistry and western blotting, respectively. Subsequently, RANBP9 -short hairpin RNA (shRNA) and RANBP9 plasmids were constructed and transfected into HCT116 and HT29 cells. The effects of RANBP9 knockdown were assessed by Cell Counting kit-8 and colony formation assays, and its effects on tumorigenicity in a nude mouse animal model were investigated. The effect of RANBP9 -shRNA on cell cycle progression was analyzed by flow cytometry, while cell cycle-associated protein expression levels were examined by western blotting. Compared with in paired normal mucosa, RANBP9 was overexpressed in CRC tissues. Inhibition of RANBP9 in HCT116 and HT29 cells significantly promoted cell growth, colony formation and S phase transition, and increased tumorigenesis in vivo . Accordingly, RANBP9 overexpression inhibited cell growth and colony formation. Knockdown of RANBP9 was associated with upregulated cyclin A2 in the two cell lines. In conclusion, RANBP9 served an inhibitory role in CRC in vitro and in vivo . Therefore, RANBP9 may be considered a potential target for treatment of CRC.

Background: Colorectal cancer (CRC) is the third most common malignancy worldwide. RANBP9 is a RAN-binding protein that has been reported to be a reliable predictor for prognosis in some human cancers. The mechanism of RANBP9 involvement in CRC carcinogenesis is unknown. This study measured RANBP9 expression levels in CRC to determine its association with clinicopathological parameters.Methods: This study included 228 CRC patients who underwent radical resection. RANBP9 expression was determined using immunohistochemistry. Based on follow-up data, the correlation of RANBP9 expression levels with clinicopathological parameters, including disease free survival (DFS) and overall survival (OS) was evaluated.Results: Reduced RANBP9 expression was correlated with tumor location (P=0.014), vascular invasion (P=0.057) and normal serum carcinoembryonic antigen levels (P=0.001). Patients with reduced RANBP9 expression had a 5-year DFS rate of 63.0% compared to 78.9% for patients with high expression levels of RANBP9 (P=0.015). Subgroup analysis demonstrated that reduced RANBP9 expression was significantly correlated with a worse DFS rate (P=0.037) for patients with left-sided colon cancer. RANBP9 was found to be an independent predictive factor for estimating DFS rate (P=0.029, hazard ratio: 0.580, 95% confidence interval: 0.356-0.946) and OS.Conclusions: RANBP9 expression levels is a potential prognostic factor for estimating CRC survival rates in patients after surgery.

BACKGROUND: The role of ELAPOR1 has been evaluated in several cancers but has not been elucidated in colorectal cancer (CRC). OBJECTIVE: To investigate the role of ELAPOR1 in CRC. METHODS: In the present study, the correlation between ELAPOR1 and survival of CRC patients in TCGA-COAD-READ datasets was predicted, and the difference in ELAPOR1 expression between tumor and normal tissues was analyzed. ELAPOR1 expression in CRC tissues was measured by immunohistochemistry. Then, ELAPOR1 and ELAPOR1-shRNA plasmids were constructed and transfected into SW620 and RKO cells. The effects were assessed by CCK-8, colony formation, transwell, and wound healing assays. Transcriptome sequencing and bioinformatics analysis were performed on the genes before and after ELAPOR1 overexpression in SW620 cells; the differentially expressed genes were substantiated by real-time quantitative reverse transcription PCR. RESULTS: High level of ELAPOR1 is associated with favorable disease-free survival and overall survival. Compared to normal mucosa, ELAPOR1 is lower in CRC. Moreover, ELAPOR1 overexpression significantly inhibits cell proliferation and invasion in vitro in SW260 and RKO cells. Conversely, ELAPOR1-shRNA promotes CRC cell proliferation and invasion. Among the 355 differentially expressed mRNAs identified, 234 were upregulated and 121 were downregulated. Bioinformatics indicated that these genes are involved in receptor binding, plasma membrane, negative regulation of cell proliferation, as well as common cancer signaling pathways. CONCLUSIONS: ELAPOR1 plays an inhibitory role in CRC and may be used as a prognostic indicator and a potential target for treatment.