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. 2018 Aug 3;9:857. doi: 10.3389/fphar.2018.00857

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Copyright © 2018 Wu, Liu, Wei, Li, Zang, Qian, Bai, Li, Xie, Zhu, Wang and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Biological role of WISP1 in pancreatic carcinogenesis. After lentivirus-mediated WISP1-overexpression vector or control (lent-WISP1 or lent-ctr) was transduced into SH-PAN cells and lentivirus-mediated WISP1-silencing vector or control (lent-WISP1 or lent-ctr) was transduced into PDAC cells, MTT assay (A), soft agar assay (B) (black bar scale = 500 μm) and Matrigel invasion assay (C) (black bar scale = 50 μm) showed the anchorage-dependent and anchorage-independent growth ability, and tumor invasion rate. The subcutaneous tumorigenic ability (D) and lung metastasis after vein injection (E) of tumor cells were measured (n = 5). HE-stained sections of lung: red arrow, metastatic nodule. ^∗P < 0.05; ^∗∗P < 0.01; ^∗∗∗P < 0.001 (black bar scale = 200 μm).