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. 2019 Aug 9;38:348. doi: 10.1186/s13046-019-1334-5

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — TET1 suppresses pancreatic cell proliferation in vitro and in vivo. a In SW1990-KO, TET1 knockout strongly accelerated cell proliferation (**P < 0.01, up CCK8, down colony formation assay). b TET1 overexpressed in BXPC-3 by TET1-OE transient transfection inhibited cell proliferation (P < 0.01, up CCK8, down colony formation assay) compared to TET1-MUT and EV transient transfection. c Flow cytometry analysis of the cell cycle distribution of SW1990-KO and BX-TET1-OE cells compared with their negative control cells, respectively (left). Data summary (*P < 0.05, right). d and e Subcutaneous tumor formation (red loops) of BX-TET1-OE and BX-TET1-NC cells. f Tumor weight comparison (**P < 0.01). g Ki-67 IHC analysis of tumors implanted in nude mice (mag. 200×, left). Data summary (**P < 0.01, right)