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. 2017 Sep 21;25(8):1383–1390. doi: 10.3727/096504017X14879366402279

Figure 5.

Figure 5

The suppression of miR-101-3p on gastric adenocarcinoma cell proliferation and invasion was associated with SRF-mediated HOTAIR expression. (A) miR-101-3p negatively regulated SRF-mediated HOTAIR expression. Upon reaching 70% confluence, AGS cells were transfected with 60 nM miR-101-3p mimics, 60 nM miR-101-3p antagomirs, 60 nM relative NCs, 40 nM siRNAs, or 2 μg of vectors. After incubation for 48 h, HOTAIR expression was detected with real-time qPCR. (B, C) Silencing of either SRF or HOTAIR counteracted the promotion of gastric adenocarcinoma cell proliferation and invasion by the miR-101-3p antagomirs. The miR-101-3p antagomirs were transfected alone or cotransfected with SRF siRNA or HOTAIR siRNA into AGS cells. After incubation for 48 h, cell proliferation and invasion were detected. *p < 0.05 versus mimic-NC, ctrl-siRNA, anta-NC, or Vector.