Y Wang1, X-L Yan, S-K Tian. 1. Department of Outpatient, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. imva56@163.com.
Abstract
OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) play an important role in tumorigenesis. In this research, lncRNA CCAT5 was explored to identify its role in the development of colorectal cancer (CRC). PATIENTS AND METHODS: Real time-quantitative polymerase chain reaction (RT-qPCR) was utilized to measure CCAT5 expression of CRC tissues. Besides, function assays including wound healing assay and transwell assay were conducted. Furthermore, RT-qPCR and Western blot assay were used to explore the underlying mechanism. RESULTS: By comparison with CCAT5 expression in adjacent tissues, the CCAT5 expression level was significantly higher in CRC samples. Moreover, after CCAT5 was downregulated, cell migration and cell invasion of CRC cells were suppressed. Besides, after knockdown of CCAT5, the mRNA and protein expression of STAT3 was repressed. Furthermore, it was found that STAT3 expression was positively correlated to CCAT5 expression in CRC tissues. CONCLUSIONS: Results suggest that CCAT5 could promote cell migration and invasion of CRC by upregulating STAT3, which may offer a potential therapeutic target in CRC.
OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) play an important role in tumorigenesis. In this research, lncRNA CCAT5 was explored to identify its role in the development of colorectal cancer (CRC). PATIENTS AND METHODS: Real time-quantitative polymerase chain reaction (RT-qPCR) was utilized to measure CCAT5 expression of CRC tissues. Besides, function assays including wound healing assay and transwell assay were conducted. Furthermore, RT-qPCR and Western blot assay were used to explore the underlying mechanism. RESULTS: By comparison with CCAT5 expression in adjacent tissues, the CCAT5 expression level was significantly higher in CRC samples. Moreover, after CCAT5 was downregulated, cell migration and cell invasion of CRC cells were suppressed. Besides, after knockdown of CCAT5, the mRNA and protein expression of STAT3 was repressed. Furthermore, it was found that STAT3 expression was positively correlated to CCAT5 expression in CRC tissues. CONCLUSIONS: Results suggest that CCAT5 could promote cell migration and invasion of CRC by upregulating STAT3, which may offer a potential therapeutic target in CRC.