Obesity-Altered Adipose Stem Cells Promote ER+ Breast Cancer Metastasis through Estrogen Independent Pathways

Sabol, Rachel A.; Beighley, Adam; Giacomelli, Paulina; Wise, Rachel M.; Harrison, Mark A.; O’Donnnell, Ben A.; Sullivan, Brianne N.; Lampenfeld, Jacob D.; Matossian, Margarite D.; Bratton, Melyssa R.; Wang, Guangdi; Collins‐Burow, Bridgette M.; Burow, Matthew E.; Bunnell, Bruce A.

doi:10.3390/ijms20061419

Cited by 25 publications

(21 citation statements)

References 53 publications

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“…Obesity can promote the transformation of adipose-derived stem cells (ASCs) into cancer-related fibroblasts (CAFs), thereby promoting the proliferation and invasive phenotype of cancer cells (37). In addition, adipose-derived stem cells can promote ER + breast cancer cell metastasis independently of estrogen signaling (38). Leptin secreted by adipose-derived stem cells promotes the growth and metastasis of ER + breast cancer by increasing the expression of ER receptor and aromatase (39).…”

Section: Molecular and Metabolic Mechanisms Underlying The Obesity-enmentioning

confidence: 99%

The Role of Metabolic Syndrome in Endometrial Cancer: A Review

2019

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Endometrial cancer is one of the most common cancers of the female reproductive system. Although surgery, radiotherapy, chemotherapy, and hormone therapy can significantly improve the survival of patients, the treatment of patients with very early lesions and a strong desire to retain reproductive function or late recurrence is still in the early stages. Metabolic syndrome (MS) is a clustering of at least three of the five following medical conditions: central obesity, high blood pressure, high blood sugar, high serum triglycerides, and low serum high-density lipoprotein (HDL). Obesity, diabetes and hypertension often coexist in patients with endometrial cancer, which increases the risk of endometrial cancer, also known as the “triple syndrome of endometrial cancer.” In recent years, epidemiological and clinical studies have found that MS associated with metabolic diseases is closely related to the incidence of endometrial cancer. However, the key molecular mechanisms underlying the induction of endometrial cancer by MS have not been elucidated to date. Characterizing the tumor metabolism microenvironment will be advantageous for achieving a comprehensive view of the molecular mechanism of metabolic syndrome associated with endometrial cancer and for providing a new target for the treatment of endometrial cancer. This review focuses on recent advances in determining the role of metabolic syndrome-related factors and mechanisms in the pathogenesis of endometrial cancer. We suggest that interfering with the tumor metabolic microenvironment-related molecular signals may inhibit the occurrence of endometrial cancer.

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Section: Molecular and Metabolic Mechanisms Underlying The Obesity-enmentioning

confidence: 99%

The Role of Metabolic Syndrome in Endometrial Cancer: A Review

2019

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“…ASC is derived of stem cells from mesenchymal lineage, and they are capable of differentiating into adipocytes, myocytes, osteocytes, or chondrocytes, which draw attention to their therapeutic potential for treating disorders or even their involvement in the development of diseases such as cancer [135]. Conditioned culture media obtained from obese-altered ASC were capable of generating MCF7 breast cancer cell metastasis through the upregulation of ABCB1 and SERPINE1 genes [136]. In prostate cancer, ASC stimulates adipocyte-induced prostate tumor growth through the activation of STAMP2 expression [137].…”

Section: Strategies To Target Cancer Stem Cellsmentioning

confidence: 99%

Cancer Stem Cells: Powerful Targets to Improve Current Anticancer Therapeutics

Bighetti‐Trevisan

Sousa

Castilho

et al. 2019

Stem Cells International

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A frequent observation in several malignancies is the development of resistance to therapy that results in frequent tumor relapse and metastasis. Much of the tumor resistance phenotype comes from its heterogeneity that halts the ability of therapeutic agents to eliminate all cancer cells effectively. Tumor heterogeneity is, in part, controlled by cancer stem cells (CSC). CSC may be considered the reservoir of cancer cells as they exhibit properties of self-renewal and plasticity and the capability of reestablishing a heterogeneous tumor cell population. The endowed resistance mechanisms of CSC are mainly attributed to several factors including cellular quiescence, accumulation of ABC transporters, disruption of apoptosis, epigenetic reprogramming, and metabolism. There is a current need to develop new therapeutic drugs capable of targeting CSC to overcome tumor resistance. Emerging in vitro and in vivo studies strongly support the potential benefits of combination therapies capable of targeting cancer stem cell-targeting agents. Clinical trials are still underway to address the pharmacokinetics, safety, and efficacy of combination treatment. This review will address the main characteristics, therapeutic implications, and perspectives of targeting CSC to improve current anticancer therapeutics.

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“…To give an example insulin/IGF-1 axis is associated with pancreatic, colorectal and prostate cancers [3]. Adipose tissue as an active endocrine organ produces many hormones including leptin which promotes tumor growth and metastasis in breast cancer through estrogen receptor alpha upregulation [4].…”

Section: Obesity and Carcinogenesismentioning

confidence: 99%