Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2021 Jul;236(7):5253-5264.
doi: 10.1002/jcp.30229. Epub 2020 Dec 23.

LDL cholesterol promotes the proliferation of prostate and pancreatic cancer cells by activating the STAT3 pathway

Young Yun Jung  1 , Jeong-Hyeon Ko  1 , Jae-Young Um  1 , Arunachalam Chinnathambi  2 , Sulaiman Ali Alharbi  2 , Gautam Sethi  3 , Kwang Seok Ahn  1
Affiliations

LDL cholesterol promotes the proliferation of prostate and pancreatic cancer cells by activating the STAT3 pathway

Young Yun Jung et al. J Cell Physiol. 2021 Jul.

Abstract

Hypercholesterolemia has been found to be closely linked with a significant increase in both cancer incidence and mortality. However, the exact correlation between serum cholesterol levels and cancer has not been completely deciphered. Here we analyzed the effect of low-density lipoprotein (LDL) cholesterol on prostate and pancreatic cancer cells. We noted that LDL induced a substantial STAT3 activation and JAK1, JAK2, Src activation in diverse prostate and pancreatic tumor cells. Moreover, LDL promoted cancer cell proliferation, migration, and invasion as well as upregulated the expression of diverse oncogenic gene products. However, deletion of LDL-activated STAT3 in LNCaP and PANC-1 cells and reduced LDL-induced cell viability. Simvastatin (SV) treatment also alleviated LDL-induced cell viability and migration ability in both the prostate and pancreatic tumor cells. These results demonstrate that LDL-induced STAT3 activation may exert a profound effect on the proliferation and survival of tumor cells.

Keywords: STAT3; invasion; low-density lipoprotein cholesterol; pancreatic cancer; prostate cancer.

PubMed Disclaimer

References

REFERENCES

    1. Aamir, K., Khan, H. U., Sethi, G., Hossain, M. A., & Arya, A. (2019). Wnt signaling mediates TLR pathway and promote unrestrained adipogenesis and metaflammation: Therapeutic targets for obesity and type 2 diabetes. Pharmacological Research, 152, 104602. https://doi.org/10.1016/j.phrs.2019.104602
    1. Acloque, H., Adams, M. S., Fishwick, K., Bronner-Fraser, M., & Nieto, M. A. (2009). Epithelial-mesenchymal transitions: The importance of changing cell state in development and disease. Journal of Clinical Investigation, 119(6), 1438-1449. https://doi.org/10.1172/JCI38019
    1. Aggarwal, B. B., Sethi, G., Ahn, K. S., Sandur, S. K., Pandey, M. K., Kunnumakkara, A. B., Sung, B., & Ichikawa, H. (2006). Targeting signal-transducer-and-activator-of-transcription-3 for prevention and therapy of cancer: modern target but ancient solution. Annals of the New York Academy of Sciences, 1091, 151-169. https://doi.org/10.1196/annals.1378.063
    1. Ahern, T. P., Pedersen, L., Tarp, M., Cronin-Fenton, D. P., Garne, J. P., Silliman, R. A., Sorensen, H. T., & Lash, T. L. (2011). Statin prescriptions and breast cancer recurrence risk: A Danish nationwide prospective cohort study. Journal of the National Cancer Institute, 103(19), 1461-1468. https://doi.org/10.1093/jnci/djr291
    1. Ahn, K. S., Sethi, G., & Aggarwal, B. B. (2007). Simvastatin potentiates TNF-alpha-induced apoptosis through the down-regulation of NF-kappaB-dependent antiapoptotic gene products: Role of IkappaBalpha kinase and TGF-beta-activated kinase-1. Journal of Immunology, 178(4), 2507-2516. https://doi.org/10.4049/jimmunol.178.4.2507

Publication types

MeSH terms

LinkOut - more resources