Abstract
MicroRNA-106b-5p (miR-106b-5p) is involved in the development of many cancers including colorectal cancer (CRC), and FAT4 is correlated with regulation of growth and apoptosis of cancer cells. The present study aimed to investigate the relation between FAT4 and miR-106b-5p and the underlying mechanism of the two on the development of CRC. Quantitative real-time PCR (qRT-PCR) assay and Western blot (WB) analysis were performed to detect the expressions of messenger RNAs (mRNAs), microRNAs (miRNAs) and proteins. The viability of CRC cells was detected by cell counting kit-8 (CCK-8). Scratch test and transwell assay were performed to measure the migration and invasion of CRC cell. Tumor angiogenesis was simulated by in vitro angiogenesis experiment. Dual-luciferase reporter assay was performed to verify the targeting relation between miR-106b-5p and FAT4. The study found that the expression of FAT4 was down-regulated and that of miR-106b-5p was up-regulated in CRC tissues. Overexpression of FAT4 resulted in decreased proliferation, migration, invasion and angiogenesis of CRC cells, whereas silencing of FAT4 led to the opposite results. In rescue experiment, miR-106b-5p partially reversed the function of FAT4 in CRC cells, thus playing a carcinogenic role by targeting FAT4 in the CRC cells.
Highlights
Colorectal cancer (CRC) still remains one of the main causes of cancer-related mortality [1,2,3]
Quantitative real-time PCR showed that the messenger RNA (mRNA) expression level of FAT atypical cadherin 4 (FAT4) was down-regulated in CRC tissues compared with normal adjacent tissues (Figure 1A). qRT-PCR and Western blot (WB) assays revealed that compared with human normal colon cell line CCD-18Co, mRNA and protein expressions of FAT4 were decreased in CRC cell lines LS174T, LOVO, HT29, HCT116 and SW-620
Our study revealed that miR-106b-5p targeting FAT4 had an anti-cancerous effect on CRC by regulating the epithelial–mesenchymal transition (EMT) process, which may provide a theoretical reference for the precise treatment of CRC
Summary
Colorectal cancer (CRC) still remains one of the main causes of cancer-related mortality [1,2,3]. Poor prognosis of CRC patients is associated with tumor metastasis [5]. Collaborative development of biomarker drugs could inhibit the development of tumors including CRC [6], further research on the molecular basis of progression and metastasis of CRC may help design new drugs for the cancer treatment. It was reported that expression of FAT4 is low-expressed in gastric cancer [9], endometrial cancer [10] and hepatocellular carcinoma [11]. A previous study found that overexpression of FAT4 promotes cell cycle, proliferation, invasion and migration of certain cancers and inhibits tumor cell apoptosis [12]. The role and mechanism of FAT4 in CRC are less reported
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