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Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling

Cumulative studies have indicated that high-dose vitamin C has antitumor effects against a variety of cancers. However, the molecular mechanisms underlying these inhibitory effects against tumorigenesis and metastasis, particularly in relation to pancreatic cancer, are unclear. Here, we report that...

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Detalles Bibliográficos
Autores principales: Kim, Ji Hye, Hwang, Sein, Lee, Ji-Hye, Im, Se Seul, Son, Jaekyoung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9603812/
https://www.ncbi.nlm.nih.gov/pubmed/36293106
http://dx.doi.org/10.3390/ijms232012249
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author Kim, Ji Hye
Hwang, Sein
Lee, Ji-Hye
Im, Se Seul
Son, Jaekyoung
author_facet Kim, Ji Hye
Hwang, Sein
Lee, Ji-Hye
Im, Se Seul
Son, Jaekyoung
author_sort Kim, Ji Hye
collection PubMed
description Cumulative studies have indicated that high-dose vitamin C has antitumor effects against a variety of cancers. However, the molecular mechanisms underlying these inhibitory effects against tumorigenesis and metastasis, particularly in relation to pancreatic cancer, are unclear. Here, we report that vitamin C at high concentrations impairs the growth and survival of pancreatic ductal adenocarcinoma (PDAC) cells by inhibiting glucose metabolism. Vitamin C was also found to trigger apoptosis in a caspase-independent manner. We further demonstrate that it suppresses the invasion and metastasis of PDAC cells by inhibiting the Wnt/β-catenin-mediated epithelial-mesenchymal transition (EMT). Taken together, our results suggest that vitamin C has therapeutic effects against pancreatic cancer.
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spelling pubmed-96038122022-10-27 Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling Kim, Ji Hye Hwang, Sein Lee, Ji-Hye Im, Se Seul Son, Jaekyoung Int J Mol Sci Article Cumulative studies have indicated that high-dose vitamin C has antitumor effects against a variety of cancers. However, the molecular mechanisms underlying these inhibitory effects against tumorigenesis and metastasis, particularly in relation to pancreatic cancer, are unclear. Here, we report that vitamin C at high concentrations impairs the growth and survival of pancreatic ductal adenocarcinoma (PDAC) cells by inhibiting glucose metabolism. Vitamin C was also found to trigger apoptosis in a caspase-independent manner. We further demonstrate that it suppresses the invasion and metastasis of PDAC cells by inhibiting the Wnt/β-catenin-mediated epithelial-mesenchymal transition (EMT). Taken together, our results suggest that vitamin C has therapeutic effects against pancreatic cancer. MDPI 2022-10-14 /pmc/articles/PMC9603812/ /pubmed/36293106 http://dx.doi.org/10.3390/ijms232012249 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kim, Ji Hye
Hwang, Sein
Lee, Ji-Hye
Im, Se Seul
Son, Jaekyoung
Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling
title Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling
title_full Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling
title_fullStr Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling
title_full_unstemmed Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling
title_short Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling
title_sort vitamin c suppresses pancreatic carcinogenesis through the inhibition of both glucose metabolism and wnt signaling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9603812/
https://www.ncbi.nlm.nih.gov/pubmed/36293106
http://dx.doi.org/10.3390/ijms232012249
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