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. 2022 Jun 10;13(6):543. doi: 10.1038/s41419-022-04993-5

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© The Author(s) 2022

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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Fig. 7 — A The human samples were collected and lysate and following by a western blot analysis with anti-LETM1, anti-PINK1 and anti-Actin antibodies. The blots were then quantified by using ImageJ software (NIH, Bethesda, MD, USA). The relative expression of indicated protein (LETM1, PINK1) was calculated by normalizing all density values to that of actin in each lane. The results are displayed as mean ± SD and are representative of three independent samples. *p < 0.05. The proposed model of the role of LETM1 overexpression in mitophagy and tumorigenesis. B Overexpression of LETM1 induces mitochondria-associated ER membrane (MAM) by interacting with GRP78 and/or GRP75 and consequently reducing Ca⁺⁺ uptake. The formation of MAM, as triggered by LETM1 overexpression, leads to mitochondrial dysfunctions such as fragmentation, defects in Ca⁺⁺ and mPTP homeostasis, and loss of MMP, resulting in mitophagy. Mitophagy induced by LETM1 overexpression in lung cancer cells is advantageous for tumorigenesis.