Prognostic factors and therapeutic effects of different treatment modalities for colorectal cancer liver metastases

BACKGROUND Colorectal cancer(CRC)is one of the most common malignant tumors in China,and the liver is the most common metastatic site in patients with advanced CRC.Hepatectomy is the gold standard treatment for colorectal liver metastases.For patients who cannot undergo radical resection of liver metastases for various reasons,ablation therapy,interventional therapy,and systemic chemotherapy can be used to improve their quality of life and prolong their survival time.AIM To explore the prognostic factors and treatments of liver metastases of CRC.METHODS A retrospective analysis was conducted on 87 patients with liver metastases from CRC treated at the Liaoning Cancer Hospital and Institute between January 2005 and March 2011.According to different treatments,the patients were divided into the following four groups:Surgical resection group(36 patients);ablation group(23 patients);intervention group(15 patients);and drug group(13 patients).The clinicopathological data and postoperative survival of the four groups were analyzed.The Kaplan-Meier method was used for survival analysis,and the Cox proportional hazards regression model was used for multivariate analysis.RESULTS The median survival time of the 87 patients was 38.747±3.062 mo,and the 1-and 3-year survival rates were 87.5%and 53.1%,respectively.The Cox proportional hazards model showed that the following factors were independent factors affecting prognosis:The degree of tumor differentiation,the number of metastases,the size of metastases,and whether the metastases are close to great vessels.The results of treatment factor analysis showed that the effect of surgical treatment was better than that of drugs,intervention,or ablation alone,and the median survival time was 48.83±4.36 mo.The drug group had the worst prognosis,with a median survival time of only 13.5±0.7 mo(P<0.05).For patients with liver metastases of CRC near the great vessels,the median survival time(27.3 mo)of patients undergoing surgical resection was better than that of patients using other treatments(20.6 mo)(P<0.05).CONCLUSION Patients with a low degree of primary tumor differentiation,multiple liver metastases(number of tumors>4),and maximum diameter of liver metastases>5 cm have a poor prognosis.Among drug therapy,intervention,ablation,and surgical treatment options,surgical treatment is the first choice for liver metastases.When liver metastases are close to great vessels,surgical treatment is significantly better than drug therapy,intervention,and ablation alone.

Sp1 contributes to overexpression of stanniocalcin 2 through regulation of promoter activity in colon adenocarcinoma

BACKGROUND Aberrant expression of stanniocalcin 2 (STC2) is implicated in colon adenocarcinoma (COAD). A previous study identified that STC2 functions as a tumor promoter to drive development of some cancers, but the role of its overexpression in the development of COAD remains unclear. AIM To evaluate the regulation mechanism of STC2 overexpression in COAD. METHODS The expression of STC2 in COAD was assessed by TCGA COAD database and GEO (GSE50760). Methylation level of the STC2 promoter was evaluated with beta value in UALCAN platform, and the correlation between STC2 expression and survival rate was investigated with TCGA COAD. Transcription binding site prediction was conducted by TRANSFAC and LASAGNA, and a luciferase reporter system was used to identify STC2 promoter activity in several cell lines, including HEK293T, NCM460, HT29, SW480, and HCT116. Western blotting was performed to evaluate the role of Sp1 on the expression of STC2. RESULTS The central finding of this work is that STC2 is overexpressed in COAD tissues and positively correlated with poor prognosis. Importantly, the binding site of the transcription factor Sp1 is widely located in the promoter region of STC2. A luciferase reporter system was successfully constructed to analyze the transcription activity of STC2, and knocking down the expression of Sp1 significantly inhibited the transcription activity of STC2. Furthermore, inhibition of Sp1 remarkably decreased protein levels of STC2. CONCLUSION Our data provide evidence that the transcription factor Sp1 is essential for the overexpression of STC2 in COAD through activation of promoter activity. Taken together, our finding provides new insights into the mechanism of oncogenic function of COAD by STC2.