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. 2020 May 23;111(7):2259–2274. doi: 10.1111/cas.14453

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© 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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The ACER2/ SMPDL3B axis regulates HCC cell growth via S1P. A‐D, Hunh‐7 cells under the indicated treatments were lysed. One portion of the lysate was subjected to an S1P ELISA (A, B). Error bars represent the SD from 3 independent experiments, and statistical significance was analyzed using Student t test (*P < .05; **P < .01; ***P < .001). The other portion of the lysate was analyzed by western blotting with the indicated antibodies (C, D). E, F, SKII rescued the cell growth mediated by ACER2 overexpression (E) or SMPDL3B overexpression in the presence of ACER2 knockdown (F). Error bars represent the SD from 3 independent experiments, and statistical significance was analyzed using Student t test (#, +P < .05; **, ## or ++P < .01; ***, ### or +++P < .001). plus sign: ACER2 shRNA + SMPDL3B vs ACER2 shRNA + SMPDL3B+SKII or GFP‐ACER2 + NC siRNA vs GFP‐ACER2 + NC siRNA + SKII (applicable below)