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. 2018 Jan 18;8:1063. doi: 10.1038/s41598-018-19599-1

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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A renewed model of v-Src-induced tumorigenesis. (a) The commonly accepted concept of v-Src-induced tumorigenesis. Expression of v-Src induces activation of downstream signaling pathways, including the ERK/MAPK pathway. Continuous expression of v-Src forces cells to proliferate uncontrollably, which leads to oncogenic transformation. (b) Our renewed model of v-Src-induced tumorigenesis. During the first 24 h after v-Src induction, all of v-Src-expressing cells exhibit (i) up-regulation of pERK and p21, (ii) cell rounding and detachment, (iii) cell cycle arrest, and (iv) chromosome abnormalities. From 24 h to 36 h after v-Src induction, v-Src-expressing cells are unable to proliferate due to continuous up-regulation of p21. However, approximately half of v-Src-expressing cells happen to suppress the level of v-Src expression, resulting in decreases of p21 and pERK to baseline levels. A limited number of cells suppressing inducible v-Src can only gain the ability to re-adhere to a culture dish, re-proliferate vigorously and finally form transformed colonies.