Abstract. The metastatic spread of tumor cells is one of the most common causes of mortality in cancer patients. The elucidation of the molecular mechanisms that underlie the formation of metastatic colonies has been one of the major objectives of cancer research. Organ-specific colonization of cancer cells is a significant and noteworthy feature of metastasis. Colorectal cancer (CRC) is one of the most common causes of cancerrelated mortality. The liver is commonly the sole site of metastasis for CRC and represents a major cause of mortality in CRC patients. However, what regulates CRC cell metastasis into liver and the reasons for the liver-specific metastasis of CRC have yet to be adequately elucidated. Recent progress provides indications and a conceptual framework with which to investigate this issue. This review evaluated experimental and clinical evidence to support a mechanistic role for circulation patterns and microvessels in liver, metastasis-related genes, chemokines and their receptors, and cellular adhesion molecules in the process of CRC liver metastasis.

Rap1 GTPase-activating protein (Rap1GAP) has been reported to serve an important role in various types of cancer by specific stimulation as a negative regulator of Rap1 activity. However, the role of Rap1GAP in colorectal cancer (CRC) has yet to be fully elucidated. The aim of the present study was to investigate the expression of Rap1GAP in CRC tissues and to elucidate its clinical significance. The expression of Rap1GAP, matrix metallopeptidase 9 (MMP-9) and E-cadherin in 227 CRC tissues and paired para-carcinoma tissues was detected by immunohistochemistry. Associations between Rap1GAP expression and clinicopathological characteristics, and between Rap1GAP expression and prognostic value (OS + DFS) in CRC were investigated. Furthermore, associations between Rap1GAP expression and MMP-9 expression, and between Rap1GAP expression and E-cadherin expression were also investigated. Rap1GAP expression was markedly downregulated in CRC tissues compared with para-carcinoma tissues. Decreased expression of Rap1GAP was significantly associated with depth of invasion, lymph node metastasis, advanced Tumor-Node-Metastasis stage and a poor prognosis in patients with CRC following surgery. Furthermore, univariate and multivariate analyses revealed that Rap1GAP was an independent poor prognostic factor for disease-free survival and overall survival. In addition, Rap1GAP expression was negatively associated with MMP-9 and positively associated with E-cadherin in 227 CRC samples. In brief, the results of the present study suggested that Rap1GAP may be involved in tumor progression in CRC and may serve as a potential target for prognostic prediction of patients with CRC.

Background. Thyroid carcinoma (THCA) is one of the most common malignancies of the endocrine system, which is usually treated by surgery combined with iodine-131 (I131) radiotherapy. Aims. This study is aimed at exploring the potential targets of I131 radiotherapy in THCA. Methods. The RNA-sequencing data of THCA in The Cancer Genome Atlas database (including 568 THCA samples) was downloaded. The differentially expressed genes (DEGs) between the tumour samples whether or not subjected to I131 radiotherapy were identified using edgeR package. Using the WGCNA package, the module that was relevant with I131 radiotherapy was selected. The intersection genes of the hub module nodes and the DEGs were obtained as hub genes, followed by the function and pathway enrichment analyses using the clusterProfiler package. Moreover, the protein-protein interaction (PPI) network for the hub genes was constructed using Cytoscape software. In addition, more important hub genes were analysed with function mining using the GenCLiP2 online tool. The qPCR analysis was used to verify the mRNA expression of more important hub genes in THCA tissues. Results. There were 500 DEGs (167 upregulated and 333 downregulated) between the two groups. WGCNA analysis showed that the green module (428 nodes) exhibited the most significant correlation with I131 radiotherapy. A PPI network was built after the identification of 53 hub genes. In the PPI network, CDH5, KDR, CD34, FLT4, EMCN, FLT1, ROBO4, PTPRB, and CD93 exhibited higher degrees, which were mainly implicated in the vascular function. The relative expression of nine mRNAs in the THCA tissues treated with I131 was lower. Conclusion. I131 radiotherapy might exert therapeutic effects by targeting CDH5, KDR, CD34, FLT4, EMCN, FLT1, ROBO4, PTPRB, and CD93 in THCA patients.

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