Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3

Guha, Prasun; Bandyopadhyaya, Gargi; Polumuri, Swamy K.; Chumsri, Saranya; Gade, Padmaja; Kalvakolanu, Dhananjaya V.; Ahmed, Hafiz

doi:10.1007/s10549-014-2912-z

Cited by 73 publications

(61 citation statements)

References 60 publications

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“…Further, BC cells expressing activated STAT3 exhibit poorer therapeutic response to neo-adjuvant chemotherapy [61], and a role of STAT3 in the maintenance of BC stemness has also been well explored [39, 62]. Guha et al demonstrated a critical role of STAT3 in apoptosis resistance and development and maintenance of CSC characteristics in breast cancer cells [63]. In other cancers, such as pancreatic cancer, STAT3 has been shown to be important in maintaining stem cell phenotypes [32].…”

Section: Discussionmentioning

confidence: 99%

Resistin potentiates chemoresistance and stemness of breast cancer cells: Implications for racially disparate therapeutic outcomes

et al. 2017

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Breast cancer (BC) continues to be the most frequently diagnosed cancer in American women, which disproportionately affects women of African-American (AA) descent. Previously, we reported greater serum levels of resistin in AA BC patients relative to Caucasian-American (CA) patients, and established its role in growth and aggressiveness of breast tumor cells. Here we have investigated the role of resistin in BC-chemoresistance. MDA-MB-231 and MDA-MB-468 BC cells of CA and AA origin, respectively, were incubated with resistin prior to doxorubicin treatment. Our data suggest that resistin conferred chemoresistance to both BC cell lines; however, the effect on AA cells was more profound. Furthermore, the resistin-induced doxorubicin-resistance was shown to occur due to suppression of apoptosis. Resistin treatment also affected the stemness of BC cells, as suggested by reduced cell surface expression of CD24, induced expression of CD44 and ALDH1, and increased capability of cells to form mammospheres. Mechanistic studies revealed that resistin-induced chemoresistance, apoptosis and stemness of BC cells were mediated through STAT3 activation. Taken together, our findings provide novel insight into the role of resistin in BC biology, and strengthen its role in racially disparate clinical outcomes.

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Section: Discussionmentioning

confidence: 99%

Resistin potentiates chemoresistance and stemness of breast cancer cells: Implications for racially disparate therapeutic outcomes

et al. 2017

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“…For this purpose, two sets of each cell monolayer were scratched using a pipette tip [29]. One set of each cell was treated with 10 mM Neu5Ac in PBS for 2 h as described above in “Neu5Ac treatment” and after washing, the cells were incubated in the complete medium for additional 24 h at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Nutrient-deprived cancer cells preferentially use sialic acid to maintain cell surface glycosylation

et al. 2015

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Cancer is characterized by abnormal energy metabolism shaped by nutrient deprivation that malignant cells experience during various stages of tumor development. This study investigated the response of nutrient-deprived cancer cells and their non-malignant counterparts to sialic acid supplementation and found that cells utilize negligible amounts of this sugar for energy. Instead cells use sialic acid to maintain cell surface glycosylation through complementary mechanisms. First, levels of key metabolites (e.g., UDP-GlcNAc and CMP-Neu5Ac) required for glycan biosynthesis are maintained or enhanced upon Neu5Ac supplementation. In concert, sialyltransferase expression increased at both the mRNA and protein levels, which facilitated increased sialylation in biochemical assays that measure sialyltransferase activity as well as at the whole cell level. In the course of these experiments, several important differences emerged that differentiated the cancer cells from their normal counterparts including resistant to sialic acid-mediated energy depletion, consistently more robust sialic acid-mediated glycan display, and distinctive cell surface vs. internal vesicle display of newly-produced sialoglycans. Finally, the impact of sialic acid supplementation on specific markers implicated in cancer progression was demonstrated by measuring levels of expression and sialylation of EGFR1 and MUC1 as well as the corresponding function of sialic acid-supplemented cells in migration assays. These findings both provide fundamental insight into the biological basis of sialic acid supplementation of nutrient-deprived cancer cells and open the door to the development of diagnostic and prognostic tools.

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“…Gal-3 has been considered a tumor-associated antigen of malignancy level in breast cancer, and is implicated in aspects, such as angiogenesis [219], adhesion [220], invasion [221], apoptosis inhibition [222], migration [223], and therapeutic resistance [224]. Chen et al, through hydrazide-based chemistry method combined with liquid chromatography tandem-mass spectrometry (LC-MS/MS), identified 72 unique N-linked glycoproteins that were significantly regulated in triple negative breast cancers, among which is LGALS3BP.…”

Section: Hypoxia Alters Cell Location Of Galectins and Interaction Wimentioning

confidence: 99%

Glycobiology Modifications in Intratumoral Hypoxia: The Breathless Side of Glycans Interaction

Silva-filho¹,

Sena²,

Lima

et al. 2017

Cell Physiol Biochem

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Post-translational and co-translational enzymatic addition of glycans (glycosylation) to proteins, lipids, and other carbohydrates, is a powerful regulator of the molecular machinery involved in cell cycle, adhesion, invasion, and signal transduction, and is usually seen in both in vivo and in vitro cancer models. Glycosyltransferases can alter the glycosylation pattern of normal cells, subsequently leading to the establishment and progression of several diseases, including cancer. Furthermore, a growing amount of research has shown that different oxygen tensions, mainly hypoxia, leads to a markedly altered glycosylation, resulting in altered glycan-receptor interactions. Alteration of intracellular glucose metabolism, from aerobic cellular respiration to anaerobic glycolysis, inhibition of integrin 3α1β translocation to the plasma membrane, decreased 1,2-fucosylation of cell-surface glycans, and galectin overexpression are some consequences of the hypoxic tumor microenvironment. Additionally, increased expression of gangliosides carrying N-glycolyl sialic acid can also be significantly affected by hypoxia. For all these reasons, it is possible to realize that hypoxia strongly alters glycobiologic events within tumors, leading to changes in their behavior. This review aims to analyze the complexity and importance of glycoconjugates and their molecular interaction network in the hypoxic context of many solid tumors.

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Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3

Cited by 73 publications

References 60 publications

Resistin potentiates chemoresistance and stemness of breast cancer cells: Implications for racially disparate therapeutic outcomes

Resistin potentiates chemoresistance and stemness of breast cancer cells: Implications for racially disparate therapeutic outcomes

Nutrient-deprived cancer cells preferentially use sialic acid to maintain cell surface glycosylation

Glycobiology Modifications in Intratumoral Hypoxia: The Breathless Side of Glycans Interaction

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