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. 2022 Feb 22;13(3):6012–6023. doi: 10.1080/21655979.2022.2042133

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© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — Depletion of FOXD3-AS1 inhibited proliferation and induced apoptosis in U87 cells. (a) Depletion of FOXD3-AS1 reduced growth of U87 cells. U87 cells transfected with FOXD3-AS1 siRNA#1 or siRNA#2 or control siRNA were seeded into 96-well plates. The MTT assay was then used to evaluate cell viability at day 0, day 3, and day 6 after seeding (N = 3, *p < 0.05). (b) Control or FOXD3-AS1 siRNA#1 or siRNA#2 was transfected into U87 cells, followed by immunoblotting to examine levels of PCNA, CDK4, CDK6, and cleaved caspase-3 in U87 cells. Actin served as the loading control. (c) The colony formation assay indicated that FOXD3-AS1 deletion suppressed cell survival in U87 cells (N = 3, *p < 0.05). (d) AO/EB staining showed that FOXD3-AS1 deletion promoted U87 cells apoptosis (N = 3, *p < 0.05). (e) TUNLE staining results revealed that FOXD3-AS1 deletion promoted U87 cells apoptosis (N = 3).