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. 2016 Feb 13;7(10):11733–11743. doi: 10.18632/oncotarget.7367

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Copyright: © 2016 Hu et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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(A) Overexpression of SRPK1 in RNAi-MALAT1 SW480 cells restored cell proliferation inhibited by MALAT1 knockdown as measured by CCK8 assay. *P < 0.05 compared to the control group (Scramle-MALAT1); **P < 0.05 compared to the control group (RNAi-MALAT1/Vector) in Day (3) and Day (4), n = 3. (B–C) Cell migration was measured by both the wound-healing assay (B) and transwell migration assay (C). Overexpression of SRPK1 in RNAi-MALAT1 SW480 cells markedly restored the cells migration. *P < 0.001 compared to the control group (Scramle-MALAT1); **P < 0.05 compared to the control group (RNAi-MALAT1/Vector), n = 3. (D) Overexpression of SRPK1 in RNAi-MALAT1 SW480 cells restored cells invasion. The invasive capability was determined using matrigel invasion chambers. *P < 0.001 compared to the control group (Scramle-MALAT1); **P < 0.001 compared to the control group (RNAi-MALAT1/Vector), n = 3.