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. 2022 Aug 5;29:56. doi: 10.1186/s12929-022-00837-8

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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. 6 — Secretory autophagy mediated release of pro-tumor factors in TME contributes to cancer progression and tumor metastasis. Both cancer and stromal cells are able to release pro-tumor factors via secretory autophagy. Autophagy-mediated release of type I collagen and fibronectin from stellate cells as well as Wnt5A, MMP2 and TGF-β1 from cancer-associated fibroblast (CAF) or TGF-β1 from tumor-associated macrophage (TAM) facilitate tumor metastasis. In addition, autophagy-regulated release of IL-8 and IL-6 derived from CAFs or HMGB1 from TAM and cancer cells leads to inflammation and cancer progression. Furthermore, TAM produced galectin-1 via secretory autophagy creates an immunosuppressive TME and enhances tumor growth, which altogether leads to cancer progression. ECM Extracellular matrix