Events

Date: 18 September 2026   Time: 11:00 - 12:00     

Location: Fogg 1.02 (Fogg building, Floor 1, meeting room

Speaker

Prof Anu Rangarajan
Dept. of Developmental Biology and Genetics,
Indian Institute of Science, Bangalore

Abstract

Mammary epithelial stem cells play essential roles in mammary gland development; their capacity for self-renewal, multipotency, and long-term persistence also makes them potential cells-of-origin for breast cancer. Conversely, cancer stem cells (CSCs), a stem-like subpopulation within tumors, contribute to tumor heterogeneity, therapy resistance and relapse. Understanding the mechanisms that regulate normal mammary stem cells may therefore provide important insights into the emergence and persistence of breast CSCs.
Our studies provided early experimental support for the stem-cell origin of cancer by demonstrating that genetic manipulation of normal breast stem/progenitor cells can transform them into cancer cells harboring CSCs. More recently, our work has identified AMP-activated protein kinase (AMPK), a central metabolic sensor, as a key regulator of cancer cell stemness and stress adaptation. We identified an AMPK–PEA15 axis that supports mammosphere formation and showed that AMPK promotes CSC maintenance, anoikis resistance, metastatic dissemination, and chemoresistance. These findings reveal unexpected pro-tumorigenic functions of AMPK, traditionally viewed primarily as a tumor suppressor, and have led us to propose the concept of a "contextual oncogene"—where the function of a metabolic regulator is shaped by the cellular adhesion state and microenvironmental context. We are now extending these studies to normal mammary gland biology using tissue-restricted AMPK knockout models. Together, our work illustrates a continuum from normal stem-cell biology to cancer stemness and highlights how energy sensor kinase can reshape cellular identity, tumor progression, and therapeutic response.