Autophagy induction impairs migration and invasion by reversing EMT in glioblastoma cells

TL;DR: It is suggested that autophagy promotes the invasion and migration of bladder cancer cells by inducing EMT through the TGF‐β1/Smad3 signaling pathway and can form a positive feedback loop to synergistically promote invasion and Migration.

Abstract: Additional file 4: Figure S4. Verification of ATG5 knockdown effect in cell line MDA-MB-231-siATG5. a The expression levels of ATG5 in MDA-MB-231cells are analyzed using western blotting (mean ± SD, **P < 0.01). b The expression levels of autophagy-related markers in MDA-MB-231cells are analyzed using western blotting (mean ± SD, *P < 0.05, **P < 0.01, *** P < 0.001). c To further verify the effect of ATG5 knockdown on autophagy, the expression LC3 is evaluated using immunocytochemistry and assessed quantitatively (mean ± SD, *P < 0.05, scale bars: 10 μm).

TL;DR: This paper aims to demonstrate the efforts towards in-situ applicability of EMMARM, as to provide real-time information about concrete mechanical properties such as E-modulus and compressive strength.

TL;DR: This review will delve into the current literature regarding the role of autophagy by exploring the major pathways of JAK2/STAT3 and PI3K/AKT/mTOR and summarizing the current therapeutic interventions and strategies for glioma treatment.

TL;DR: The identification of Snail, ZEB and some basic helix-loop-helix factors as inducers of epithelial–mesenchymal transition (EMT) and potent repressors of E-cadherin expression has opened new avenues of research with potential clinical implications.

TL;DR: The EMT-associated reprogramming of cells not only suggests that fundamental changes may occur to several regulatory networks but also that an intimate interplay exists between them.

TL;DR: This review discusses the cellular process of autophagy (“self-eating”), which plays key roles in normal development of the immune system and adaptation to stress, as well as in a wide range of disease states.

TL;DR: It is shown that heterozygous disruption of beclin 1 increases the frequency of spontaneous malignancies and accelerates the development of hepatitis B virus-induced premalignant lesions, providing genetic evidence that autophagy is a novel mechanism of cell-growth control and tumor suppression.