Dietary fat increases solid tumor growth and metastasis of 4T1 murine mammary carcinoma cells and mortality in obesity-resistant BALB/c mice

Kim, Young Ho; Choi, Mi Ran; Park, Heesook; Kim, Minhee; Hong, Juhee; Lee, Jae Yong; Chun, Hyang Sook; Lee, Ki Won; Park, Jung Han Yoon

doi:10.1186/bcr2927

Cited by 106 publications

(102 citation statements)

References 45 publications

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“…Furthermore, the conditioned media from preadipocyte-derived adipocytes, but not that from undifferentiated preadipocytes, increased MCF-7 cell proliferation (35). Dietary fat increases mammary tumor growth and metastasis, thereby increasing the risk of mortality in obesity-resistant mice (36). Leptin has been implicated in breast cancer development as a determinant for the tumorpromoting activity of cancer-associated fibroblasts (CAFs) in breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Leptin promotes the proliferation and migration of human breast cancer through the extracellular-signal regulated kinase pathway

Sun

2013

Molecular Medicine Reports

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Abstract. Obesity has been associated with an increased risk of postmenopausal breast cancer, which may be due to the expression of leptin. The aim of this study was to determine the role of leptin in the growth of breast cancer cells in nude mice, the proliferation and migration of MCF-7 human breast cancer cells and its downstream signaling pathway. The xenograft mouse model was elicited by injecting MCF-7 human breast cancer cells into the left back axilla and the tumor size was measured every other day. Leptin injected subcutaneously around the tumor site led to an increase in the size and weight of the tumor, whereas the leptin antagonist (LA) significantly inhibited the size and weight of the tumor. Leptin promoted the proliferation and migration of MCF-7 cells and LA inhibited it. The effects of leptin on increasing the size and weight of the tumor in the nude mice and the proliferation and migration of MCF-7 human breast cancer cells were eradicated by pretreatment with LA, the extracellular-signal regulated kinase (ERK) inhibitor PD98059. In the xenograft mouse model the leptin level was increased and leptin increased the phosphorylation of ERK in the MCF-7 cells, whereas LA significantly reduced the phosphorylation of ERK. These results indicated that leptin promotes the growth of breast cancer in the nude mice and increases the proliferation and migration of MCF-7 human breast cancer cells via the ERK pathway.

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Section: Discussionmentioning

confidence: 99%

Leptin promotes the proliferation and migration of human breast cancer through the extracellular-signal regulated kinase pathway

Sun

2013

Molecular Medicine Reports

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“…Is it a consequence of obesity or do the causes of obesity independently promote the carcinogenic process? In response to this intriguing question, it is interesting to note that multiple models have now been reported wherein transplanted and/or spontaneous tumors, including breast cancer, are promoted by high-fat diet in the absence of obesity (26)(27)(28)(29)(30).…”

Section: Articles By Iyengar Et Al Published In This Issue Cancer Prmentioning

confidence: 99%

Crown-like Structures in Breast Adipose Tissue from Normal Weight Women: Important Impact

Berger

2017

Cancer Prevention Research

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Crown-like structures (CLS), composed of macrophages surrounding dead or dying adipocytes, are a histologic hallmark of the proinflammatory process by which adipose tissue contributes to the increased risk and worse prognosis of breast cancer in obese, postmenopausal patients. In this issue of Cancer Prevention Research, Iyengar and colleagues report the intriguing finding that CLS can be identified in a significant proportion of normal-BMI women undergoing mastectomy for breast cancer risk reduction or therapy. This surprising observation suggests that some normal weight women may have similar mechanisms driving initiation and/or progression of breast cancer as those contributing to the increased incidence and worse prognosis of breast cancer in obese postmenopausal women. The possibility of a common mechanism in both lean and obese women provides added impetus to more fully define this process and evaluate its important implications for prevention and screening strategies as well as therapeutic interventions. Cancer Prev Res; 10(4); 223-5. Ó2017AACR.

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“…All migration and invasion assays were repeated at least 3 times. The viability of cells was estimated as previously described (22).…”

Section: Transwell Migration and Invasion Assaysmentioning

confidence: 99%

Licochalcone E Present in Licorice Suppresses Lung Metastasis in the 4T1 Mammary Orthotopic Cancer Model

Kwon

Park

Kwon

et al. 2013

Cancer Prevention Research

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We investigated whether licochalcone E (LicE), a phenolic constituent of licorice, inhibits mammary tumor growth and metastasis using animal and cell culture models. 4T1 mammary carcinoma cells were injected into the mammary fat pads of syngeneic BALB/c mice. Starting 7 days after the injection, the mice received LicE (7 or 14 mg/kg body weight/day) via oral gavage for 25 days. LicE suppressed solid tumor growth and lung metastasis, but did not exhibit kidney or liver toxicity. In tumor tissues, LicE treatment induced a reduction in the expression of Ki67, cyclins, and cyclin-dependent kinases and stimulated apoptosis with increased expression of Bax and cleaved caspase-3 but decreased expression of Bcl-2. In addition, LicE decreased expression of CD31, vascular endothelial growth factor (VEGF)-A and C, VEGFreceptor 2, lymphatic vessel endothelial receptor-1, CD45, cyclooxygenase-2, inducible nitric oxide synthase, and hypoxia inducible factor-1a in tumor tissues. In lung tissues, LicE reduced the levels of proinflammatory cytokines and angiogenesis/metastasis-related proteins. In mammary cancer cell cultures, LicE (5-20 mmol/L) dose dependently inhibited cell migration and invasion. LicE inhibited secretion of matrix metalloproteinase-9, urokinase-type plasminogen activator and VEGF-A, and stimulated secretion of tissue inhibitor of metalloproteinase-2 in MDA-MB-231 cells. In addition, LicE inhibited tube formation of vascular endothelial cells. We show that LicE administration suppressed tumor growth and lung metastasis in the mouse model in conjunction with LicE inhibition of cell migration, invasion, and tube formation in vitro. Reduced tumor growth and metastasis in LicE-treated mice may be, at least in part, attributed to reduced inflammation and tumor angiogenesis. Cancer Prev Res; 6(6); 603-13. Ó2013 AACR.

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Dietary fat increases solid tumor growth and metastasis of 4T1 murine mammary carcinoma cells and mortality in obesity-resistant BALB/c mice

Cited by 106 publications

References 45 publications

Leptin promotes the proliferation and migration of human breast cancer through the extracellular-signal regulated kinase pathway

Leptin promotes the proliferation and migration of human breast cancer through the extracellular-signal regulated kinase pathway

Crown-like Structures in Breast Adipose Tissue from Normal Weight Women: Important Impact

Licochalcone E Present in Licorice Suppresses Lung Metastasis in the 4T1 Mammary Orthotopic Cancer Model

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