# From Hero to Hijacker: Autophagy’s Double Life in Immune Patrols and Cancer Escape

## TL;DR

This paper explores how autophagy helps cells respond to mechanical stress, playing a key role in both immune cell movement and cancer spread.

## Contribution

The paper highlights the dual role of autophagy-related proteins in immune patrols and cancer escape under mechanical stress.

## Key findings

- Mechanical stress modulates autophagy initiation and lysosomal function across cell types.
- Autophagy-related pathways are crucial for leukocyte diapedesis and tumor cell extravasation.
- ATGs have dual roles in cytoplasmic degradation and secretory functions under stress.

## Abstract

Cells are constantly exposed to mechanical forces that shape their behavior, survival, and fate. The autophagy machinery emerges as a central adaptive pathway in these processes, acting not only as a metabolic and quality control mechanism but also as a key regulator of membrane dynamics and mechanotransduction. Here, we review how mechanical stress influences autophagy initiation, autophagosome maturation, and lysosomal function across different cell types. We discuss parallels between leukocyte diapedesis and circulating tumor cell (CTC) extravasation, two processes that involve profound mechanical challenges and rely on autophagy-related pathways to maintain cell integrity and enable transendothelial migration. Special attention is given to the dual role of autophagy-related proteins (ATGs) in these contexts, ranging from cytoplasmic degradation dependent on lysosomal fusion to secretory functions. Understanding how mechanical forces modulate autophagy and ATG-dependent pathways may reveal novel insights into immune regulation, tumor dissemination, and potential therapeutic targets aimed at controlling inflammation and metastasis.