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. 2022 May 7;17:20. doi: 10.1186/s13027-022-00434-2

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 1 — M.tb promotes proliferation and migration of A549 cells. BCG induces SHH signaling-dependent expression of COP1, which targets and degrades of P53, and it inhibits cell apoptosis of A549. PtpA-expressing BCG can promote proliferation and migration of A549 cells, partially through targeting GADD45A or ncRNA genes (such as miR-488, CASC2, and miR-622) which are related to tumor progression through regulating cell apoptosis, proliferation, and migration. NOX4-p62 might serve as a driving factor of the tumor microenvironment changed by tuberculosis fibrosis. Mce2E of M.tb can inhibit eEF1A1, which increase cell proliferation. These actions all promote proliferation and migration of A549