Objective: Long noncoding RNAs (lncRNAs) are critical regulators in diverse human cancers. However, the role of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in colon cancer remains to be further investigated. We aimed to verify the role of NEAT1/let-7 g-5p/BTB and CNC homology 1 (BACH1) axis in colon cancer development.
Methods: Expression of NEAT1, let-7 g-5p and BACH1 in colon cancer tissues and cells was determined. The interactions between NEAT1 and let-7 g-5p, and between let-7 g-5p and BACH1 were assessed. The colon cancer cell lines were treated with plasmids or oligonucleotides to alter NEAT1, BACH1 and let-7 g-5p expression. Then, viability, migration, invasion, and apoptosis of colon cells were evaluated, and the cell growth in vivo was observed as well.
Results: NEAT1 and BACH1 were upregulated while let-7 g-5p was downregulated in colon cancer tissues and cells. NEAT1/BACH1 silencing or let-7 g-5p elevation suppressed colon cancer cell growth in vivo and in vitro. The effects of silenced NEAT1 on colon cancer cells and xenografts were reversed by downregulating let-7 g-5p. Down-regulation of BACH1 reversed the effect of NEAT1 overexpression on colon cancer cells. NEAT1 directly bound to let-7 g-5p and let-7 g-5p targeted BACH1.
Conclusion: Downregulated NEAT1 elevated let-7 g-5p to suppress EMT of colon cancer cells through inhibiting BACH1. This research may contribute to treatment of colon cancer.
Keywords: Apoptosis; Btb and cnc homology 1; Colon cancer; Long non-coding rna nuclear paraspeckle assembly transcript 1; Microrna let-7 g-5p; Proliferation.
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