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Novel role of LLGL2 silencing in autophagy: reversing epithelial-mesenchymal transition in prostate cancer. | LitMetric

Novel role of LLGL2 silencing in autophagy: reversing epithelial-mesenchymal transition in prostate cancer.

Biol Res

Department of Veterinary Medicine, Institute of Veterinary Science, College of Veterinary Medicine, Chungnam National University, 99 Daehak-ro, Yusung-gu, Daejeon, 34134, Republic of Korea.

Published: May 2024

AI Article Synopsis

  • - Prostate cancer (PCa) is a significant health issue for men, and LLGL2, a tumor suppressor, plays an unclear role in its development, particularly in the context of epithelial-mesenchymal transition (EMT) and autophagy.
  • - Researchers conducted experiments on PC3 cells and found that reducing LLGL2 levels increases autophagy, inhibits EMT markers, and alters tumor behavior in a mouse model.
  • - The study concludes that low LLGL2 expression enhances autophagy and reduces EMT in PCa, suggesting that targeting LLGL2 may provide new strategies for treatment.

Article Abstract

Purpose: Prostate cancer (PCa) is a major urological disease that is associated with significant morbidity and mortality in men. LLGL2 is the mammalian homolog of Lgl. It acts as a tumor suppressor in breast and hepatic cancer. However, the role of LLGL2 and the underlying mechanisms in PCa have not yet been elucidated. Here, we investigate the role of LLGL2 in the regulation of epithelial-mesenchymal transition (EMT) in PCa through autophagy in vitro and in vivo.

Methods: PC3 cells were transfected with siLLGL2 or plasmid LLGL2 and autophagy was examined. Invasion, migration, and wound healing were assessed in PC3 cells under autophagy regulation. Tumor growth was evaluated using a shLLGL2 xenograft mouse model.

Results: In patients with PCa, LLGL2 levels were higher with defective autophagy and increased EMT. Our results showed that the knockdown of LLGL2 induced autophagy flux by upregulating Vps34 and ATG14L. LLGL2 knockdown inhibits EMT by upregulating E-cadherin and downregulating fibronectin and α-SMA. The pharmacological activation of autophagy by rapamycin suppressed EMT, and these effects were reversed by 3-methyladenine treatment. Interestingly, in a shLLGL2 xenograft mouse model, tumor size and EMT were decreased, which were improved by autophagy induction and worsened by autophagy inhibition.

Conclusion: Defective expression of LLGL2 leads to attenuation of EMT due to the upregulation of autophagy flux in PCa. Our results suggest that LLGL2 is a novel target for alleviating PCa via the regulation of autophagy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11077766PMC
http://dx.doi.org/10.1186/s40659-024-00499-wDOI Listing

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