Background OSBPL3 is overexpressed in a variety of malignancies and is closely associated with tumor growth and metastasis. However, its expression and function in colorectal cancer (CRC) are unclear. We aimed to investigate its prognostic and therapeutic value in this disease by detecting its expression in CRC and its correlation with the clinicopathological characteristics and prognosis of patients. Methods A total of 92 CRC samples were included in this study. According to the 2020 WHO diagnostic criteria, the criteria of the American Joint Committee on Cancer (AJCC) 8th edition staging system were used. OSBPL3 and Ki-67 expression in these samples was detected by immunohistochemistry. OSBPL3 mRNA expression was detected by qRT-PCR. KRAS/NRAS mutations were detected by an amplification refractory mutation system (ARMS). Data analysis was performed using the statistical analysis software Prism 8. Results OSBPL3 was found to be significantly overexpressed in CRC tumor tissues and was associated with worse progression-free survival and overall survival in patients. Additionally, OSBPL3 expression was negatively correlated with the degree of tumor differentiation. KRAS mutations were detected in approximately 32.6% of patients and were significantly associated with high OSBPL3 expression. In addition, OSBPL3 and Ki-67 expression was significantly correlated. Conclusions OSBPL3 is highly expressed in CRC samples and predicts a worse prognosis. OSBPL3 may become a new potential therapeutic target for CRC.

Background Hepatitis B virus X protein ( XTP1 ) is overexpressed in tumor tissues and regulates cancer progression. However, the molecular mechanism of XTP1 in gastric cancer (GC) is poorly understood. Hence, we aimed to dissect the underlying role of XTP1 in the development of GC. Methods Lentiviruses were constructed and transfected into GC cells to upregulate or downregulate gene expression. The expressions of proteins in GC cells or tumor tissues were assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR), Western blotting, immunohistochemistry (IHC) assay, or the Gene Expression Profiling Interactive Analysis (GEPIA) database. Cell proliferation was assessed via methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay, Celigo cell counting assay, cell cycle analysis, and colony formation assay. Cell apoptosis was assessed by flow cytometry. The apoptosis-related proteins were evaluated using the human apoptosis antibody array. GC cell migration was detected by scratch wound-healing assays and Transwell migration assays. Potential downstream molecules were identified by the human GeneChip assay combined with bioinformatics analysis. Results We found that XTP1 is overexpressed in GC tissues and is positively related to its pathological grade. XTP1 knockdown restrained the growth and migration of GC cells, while XTP1 overexpression promoted cell proliferation and suppressed apoptosis. A mechanistic study indicated that XTP1 knockdown inhibited cyclin-dependent kinase 6 ( CDK6 ) expression and that CDK6 might be a potential downstream molecule of XTP1 . Further study confirmed that CDK6 depletion also suppressed GC cell proliferation and migration and increased GC cell apoptosis. Moreover, rescue experiments verified that CDK6 knockdown abated the promotion of XTP1 overexpression on GC progression. Conclusions XTP1 facilitated the development and progression of GC cells by activating CDK6 . Therefore, the XTP1-CDK6 axis might be a potential therapeutic target for GC.