Epithelial–mesenchymal transition Puns

https://doi.org/10.1080/01635581.2021.1971268

https://pubmed.ncbi.nlm.nih.gov/34459685

Sorry but there is not even an abstract available.

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Open Access: False

Authors: Carly Bess Scalise - Lyse Norian - Wendy Demark-Wahnefried -

Additional links: None found

Ghahremani H, Nabati S, Tahmori H, Peirouvi T, Sirati-Sabet M, Salami S. Long-Term Glucose Restriction with or without β-Hydroxybutyrate Enrichment Distinctively Alters Epithelial-Mesenchymal Transition-Related Signalings in Ovarian Cancer Cells [published online ahead of print, 2020 Aug 16]. Nutr Cancer. 2020;1-19. doi:10.1080/01635581.2020.1804947

https://doi.org/10.1080/01635581.2020.1804947

Abstract

The beneficial impacts of the ketogenic diet and metabolic reprograming were recently reported for ovarian cancer patients. In this study, the effects of glucose restriction with or without beta-hydroxybutyrate (bHB) enrichment were studied in drug-resistant CD133high A2780CP and CD133low SK-OV-3 ovarian cancer cells to scrutinize the impact of experimental ketosis on ATP production, epithelial to mesenchymal transition (EMT), and related signaling pathways including Wnt, Hippo, and Hedgehog. Cells were adapted and maintained for a month with restricted levels of glucose (250 mg/l) with or without the therapeutic concentration of bHB (5 mM). Quantitative PCR, Western blot analysis, flow cytometry, chemiluminescence, and wound healing assay were used in this study. Glucose restriction and bHB enrichment reduced the stemness marker and diminished In Vitro migration in both cell lines. Glucose restriction significantly reduced ATP levels in both cells, but bHB enrichment was partially compensated for the ATP levels solely in SK-OV-3 cells. Glucose restriction mainly inhibited the Wnt pathway in the CD133high A2780CP cells, but the Hedgehog pathway was the main target in CD133low SK-OV-3 cells. In Conclusion, Prior targeted evaluations of key genes' expression would help to predict the distinctive impacts of metabolic fuels and to optimize the efficacy of ketogenic diets.

Yang T, Zhou Y, Wang H, et al. Insulin exacerbated high glucose-induced epithelial-mesenchymal transition in prostatic epithelial cells BPH-1 and prostate cancer cells PC-3 via MEK/ERK signaling pathway [published online ahead of print, 2020 Jun 16]. Exp Cell Res. 2020;112145. doi:10.1016/j.yexcr.2020.112145

https://doi.org/10.1016/j.yexcr.2020.112145

Abstract

As two most common progressive diseases of aging, type 2 diabetes mellitus (T2DM) and benign prostatic hyperplasia (BPH) were all characterized by endocrine and metabolic disorders. Here, our clinical study showed that there were significant differences in fasting blood glucose (FBG), fasting insulin (FINS), insulin resistance index (HOMA-IR) and prostate volume (PV) between simple BPH patients and BPH complicated with T2DM patients. Further analysis showed that HOMA-IR was positively correlated with PV in BPH complicated with T2DM patients. The in vitro experiment results showed that high glucose (HG) promoted EMT process in a glucose-dependent manner in human prostate hyperplasia cells (BPH-1) and prostate cancer cells (PC-3), and this pathological process was exacerbated by co-culture with insulin. Mechanistically, insulin-induced exacerbation of EMT was depended on the activation of MEK/ERK signaling pathway, and we suggested that insulin and its analogs should be used very carefully for the clinical antihyperglycemic treatment of BPH complicated with T2DM patients.