RESUMO
OBJECTIVE: Research has proven that the expression of CDC6 is tightly related to tumorigenesis and progression of various tumors. However, the effects of CDC6 in hepatocellular carcinoma remain uncertain. The main purpose of this research is to explore this relationship. METHODS: We assessed the expression levels of CDC6 in a serious of cancers from GEPIA database. The expression of CDC6 in hepatocellular carcinoma tissue and normal liver tissue was compared, and further assessed by immunohistochemical staining. Graphpad software was performed for data analysis, and t-test and χ2 analysis were used to investigate the role of CDC6 in hepatocellular carcinoma. RESULTS: The expression level of CDC6 was significantly higher in malignant carcinoid, melanoma, urothelial tumor, and hepatocellular carcinoma in the GEPIA online database. It was related to clinical progression of hepatocellular carcinoma. We found that the expression of CDC6 was correlated with tumor size (P=0.018) and the number of tumor nodes (P=0.003), but not with age, gender and AFP value (P>0.05). CONCLUSIONS: The expression level of CDC6 in hepatocellular carcinoma is related tightly to clinical findings. Detecting the expression of CDC6 might provide a new biomarker for patients with hepatocellular carcinoma.
RESUMO
Gastric cancer (GC) is the fourth most common malignancy worldwide, with 80% mortality rate in over 70% countries. Recently, targeted therapy for GC has great clinical prospects, and it is still badly needed to find novel molecular targets to control the progression and development of GC. Kinesin family member 3B (KIF3B) is known as a microtubule motor kinesin and one of the most ubiquitously expressed KIFs. KIF3B participates in multiple cellular processes such as mitosis and spermatogenesis, and the possible role of KIF3B on tumor progression has been widely revealed. KIF3B affects the progression and metastasis of multiple types of tumors, such as pancreatic cancer, prostate cancer, and hepatocellular carcinoma; however, its potential impact on GC is still unknown. Herein, we explored the possible role of KIF3B on the progression of GC and noticed that KIF3B was high expression in tumor tissues from GC patients. KIF3B was also significantly correlated with clinical pathological characteristics such as tumor size (P = .014*) and recurrence (P = .044*). We further revealed that KIF3B depleted GC cells exhibited impaired proliferation capacity in vitro. Similarly, KIF3B depletion suppressed tumor growth of GC cells in mice. In conclusion, we identified KIF3B as a promising therapeutic target for the treatment of GC.
