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. 2019 Dec 27;19:1252. doi: 10.1186/s12885-019-6474-7

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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. 3 — In vitro and in vivo assays. a. he protein level of AGGF1 in one normal colorectal mucosa cell line (FHC) and seven CRC cell lines. The expression level of AGGF1 protein in HCT-116 and RKO cells transfected with AGGF1 overexpression or knockdown vectors was validated using western blotting (b). GAPDH was used to normalize protein level. In vitro, overexpression or knockdown of AGGF1 inhibited or elevated CRC wound healing (c), migration, and invasion (d), respectively, compared with control groups. Upregulation or knockdown of AGGF1 expression facilitated or suppressed the tumor metastasis ability of CRC cells in nude mice. e. Representative images of metastatic tumor colonies in mice (left panel (non-metastasis): the nude mouse without metastatic tumor colonies formed, right panel (metastasis): the nude mouse with metastatic tumor colonies formed). f. HE staining of the metastatic tumor colonies in lung and liver (colored arrows: metastatic tumor colonies). g. The number of metastatic tumor colonies was counted (*p < 0.05, c, f: Original magnification: 100×; d: Original magnification: 200×)