Background: Long non-coding RNA colorectal neoplasia differentially expressed (lncRNA CRNDE) and microRNA-126-5p (miR-126-5p) were reported to be related to the development of colorectal carcinoma (CRC). However, the detailed mechanism of CRNDE and miR-126-5p is not fully understood. The purpose of this research was to explore their roles and molecular mechanism in CRC.
Methods: Quantitative real-time polymerase chain reaction was performed to detect the transcription levels of genes. Paclitaxel (PTX) was used to analyze cell drug resistance. 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and flow cytometry analysis were employed to assess cell proliferation and apoptosis, respectively. Furthermore, cell migratory and invasive abilities were measured using transwell assay. The interaction between miR-126-5p and CRNDE or ATPase family AAA domain-containing protein 2 (ATAD2) was predicted by online tool starbase and then confirmed using the dual-luciferase reporter assay. Besides, Western blot assay was carried out to detect the levels of proteins.
Results: CRNDE and ATAD2 expressions were upregulated and miR-126-5p expression was downregulated in CRC tissues and cells. CRNDE depletion repressed PTX resistance and the growth of CRC cells. Interestingly, we found that miR-126-5p was a target gene of CRNDE, and miR-126-5p directly targeted ATAD2. Furthermore, CRNDE affected CRC cell progression via modulation of miR-126-5p/ATAD2 axis in CRC cells.
Conclusion: Our data suggested that CRNDE regulated CRC cell development and PTX resistance by modulating miR-126-5p/ATAD2 axis, providing the theoretical basis for the treatment of CRC patients.
Keywords: CRNDE, miR-126-5p, ATAD2, PTX resistance, cell progression, colorectal carcinoma