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• W1993842564 abstract "A cancer stem cell has been defined as a cell within a tumor that possesses the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor. These tumor-forming cells could hypothetically originate from stem, progenitor, or differentiated cells. Previously, we have shown that breast cancer cells with low metastatic potential can be induced into a reversible state of dormancy by farnesyl transferase inhibitors (FTIs). Dormancy was induced by changes in RhoA and RhoC GTPases. Specifically, RhoA was found to be hypoactivated while RhoC was hyperactivated. In the current study we demonstrate that these dormant cells also express certain known stem cell markers such as aldehyde dehydrogenase I (ALDHI) and cluster of differentiation 44 (CD44). We also show that autophagy markers Atg5, Atg12, and LC3-B are expressed in these dormant stem cell-like breast cancer cells. Inhibiting autophagy by inhibitor 3-methyladenine (3-MA) blocked the process of autophagy reversing the dormant phenotype. Further, we show that c-jun NH2 terminal kinase (JNK/SAPK) is upregulated in these dormant stem cell-like breast cancer cells and is responsible for increasing autophagy." @default.
• W1993842564 created "2016-06-24" @default.
• W1993842564 creator A5000502057 @default.
• W1993842564 creator A5068010437 @default.
• W1993842564 date "2011-07-07" @default.
• W1993842564 modified "2023-10-18" @default.
• W1993842564 title "Breast Cancer Stem Cells Survive Periods of Farnesyl-Transferase Inhibitor-Induced Dormancy by Undergoing Autophagy" @default.
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• W1993842564 doi "https://doi.org/10.1155/2011/362938" @default.
• W1993842564 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3199942" @default.
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