n/a
Abstract Title:

Dietary Piperine Suppresses Obesity-Associated Breast Cancer Growth and Metastasis by Regulating the miR-181c-3p/Axis.

Abstract Source:

J Agric Food Chem. 2021 Dec 29 ;69(51):15562-15574. Epub 2021 Dec 14. PMID: 34905918

Abstract Author(s):

Dheeran Rajarajan, Jagadish Natesh, Dhanamjai Penta, Syed Musthapa Meeran

Article Affiliation:

Dheeran Rajarajan

Abstract:

Adipocyte-derived leptin activates multiple oncogenic signaling, leading to breast cancer cell progression and metastasis. Hence, finding effective strategies to inhibit the oncogenic effects of leptin would provide a novel approach for disrupting obesity-associated breast cancer. In the current study, we explored the role of piperine, a major plant alkaloid from(black pepper), against leptin-induced breast cancer. Piperine treatment significantly inhibited leptin-induced breast cancer cell proliferation, colony formation, migration, and invasion. We found that piperine downregulated the expression of, a predicted target of miR-181c-3p. Mechanistically, piperine potentiates miR-181c-3p-mediated anticancer potential in leptin-induced breast cancer cells. Interestingly, the knockdown ofreduced the proliferative potential of leptin-induced breast cancer cells. Further, oral administration of piperine inhibited breast tumor growth in diet-induced obese mice, accompanied by the upregulation of miR-181c-3p and downregulation ofexpression. Together, piperine represents a potential candidate for further development as an anticancer agent for treating obesity-associated breast cancer.

Print Options


Key Research Topics

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2024 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.