MicroRNA-106b-5p (miR-106b-5p) is involved in the development of many cancers including in colorectal cancer (CRC), and FAT4 is correlated with regulation of growth and apoptosis of cancer cells. This 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 mRNAs, miRNA 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.

Background. Radix Actinidiae extract (RAE) has been shown to inhibit cancer in many studies, but its potential mechanism in nasopharyngeal cancer (NPC) progression remains unclear. Methods. NPC cells (SUNE1) were treated with different doses of RAE. For transfection, SUNE1 cells were transfected with the microRNA (miR)-205-5p inhibitor (anti-miR-205-5p) or mimic followed by treatment with 200 μg/mL RAE for 24 h. The MTT assay and colony formation assay were used to detect cell proliferation and radiosensitivity. The transwell assay was used to detect cell migration and invasion. The expression of miR-205-5p was detected by quantitative real-time PCR. The protein expression levels of matrix metalloproteinase-2 (MMP2) and matrix metalloproteinase-9 (MMP9) were detected by western blot analysis. Results. RAE inhibited NPC cell proliferation, migration, and invasion, while it enhanced radiosensitivity ( P < 0.05 ). Also, RAE treatment decreased miR-205-5p expression, as well as MMP2 and MMP9 protein levels ( P < 0.05 ). Anti-miR-205-5p transfection enhanced the effects of RAE on NPC cell proliferation, migration, invasion, and radiosensitivity ( P < 0.05 ), while miR-205-5p mimic transfection had an opposite effect ( P < 0.05 ). Conclusion. RAE might decrease miR-205-5p, thereby it inhibited NPC cell proliferation and metastasis and enhanced radiosensitivity.