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The impact of DAPK1 and mTORC1 signaling association on autophagy in cancer

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Abstract

Background

The autophagy pathway is used by eukaryotic cells to maintain metabolic homeostasis. Autophagy has two functions in cancerous cells which could inhibit tumorigenesis or lead to cancer progression by increasing cell survival and proliferation.

Methods and results

In this review article, Web of Science, PubMed, Scopus,  and Google Scholar were searched and summarized published studies to explore the relationship between DAPK1 and mTORC1 signaling association on autophagy in cancer. Autophagy is managed through various proteins including the mTOR, which is two separated structural and functional complexes known as mTORC1 and mTORC2. MTORC1 is an important component of the regulatory pathway affecting numerous cellular functions including proliferation, migration, invasion, and survival. This protein plays a key role in human cancers. The activity level of mTORC1 is regulated by the death-associated protein kinases (DAPks) family, especially DAPK1. In many cancers, DAPK1 acts as a tumor suppressor which can be attributed to its ability to suppress cellular transformation and to inhibit metastasis.

Conclusions

A deep investigation not only will reveal more about the function of DAPK1 but also might provide insights into novel therapies aimed to modulate the autophagy pathway in cancer and to achieve better cancer therapy.

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Authors

Contributions

PM: conception & design of study and writing the manuscript, MS and AS: review & editing and writing the manuscript, ZA and FK: writing the manuscript, HT: supervision and validation.

Corresponding author

Correspondence to Hossein Teimori.

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The authors report no conflict of interest.

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This study does not contain any studies with human participants or animals performed by any of the authors.

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Movahhed, P., Saberiyan, M., Safi, A. et al. The impact of DAPK1 and mTORC1 signaling association on autophagy in cancer. Mol Biol Rep 49, 4959–4964 (2022). https://doi.org/10.1007/s11033-022-07154-1

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  • DOI: https://doi.org/10.1007/s11033-022-07154-1

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