Leptin and high glucose stimulate cell proliferation in MCF-7 human breast cancer cells: reciprocal involvement of PKC-α and PPAR expression

Okumura, M.; Yamamoto, Mayumi; Sakuma, Hajime; Kojima, Toshihiro; Maruyama, Takako; Jamali, Marjan; Cooper, Denise R.; Yasuda, Keigo

doi:10.1016/s0167-4889(02)00276-8

Cited by 192 publications

(163 citation statements)

References 37 publications

Supporting

Mentioning

143

Contrasting

Unclassified

Order By: Relevance

“…The serum adiponectin level was found to be inversely associated with the glucose level (63). High glucose levels may amplify the mitogenic and proliferative effects of leptin on mammary epithelial cells, and stimulate the proliferation of breast cancer cells (64). In addition, adiponectin directly inhibits the proliferation of vascular smooth muscle cells (65).…”

Section: Insulin Resistance Insulin-like Growth Factor 1 (Igf-1) Andmentioning

confidence: 99%

Triple‑negative breast cancer and its?association with obesity (Review)

Zou

Chen

et al. 2017

mol clin onc

View full text Add to dashboard Cite

Abstract. Triple-negative breast cancer (TNBC) is a subtype of breast cancer that lacks expression of the estrogen and progesterone receptor and does not overexpress human epidermal growth factor 2 receptor protein. TNBC is associated with special characteristics, including aggressiveness, poor prognosis and poor response to treatment, and has been attracting increasing attention worldwide. Obesity is a well-documented factor exerting a significant effect on the development of breast cancer, including TNBC. The purpose of the present review was to focus on the association between obesity and TNBC and provide a summary of novel research findings. The aim was to highlight the association between TNBC and obesity and provide an overview of novel outlooks on clinical issues, biological rationale, novel targeted therapies and prognosis, in order to draw attention to the significance of weight management, primary prevention, early diagnosis and treatment of this intractable disease.

show abstract

Section: Insulin Resistance Insulin-like Growth Factor 1 (Igf-1) Andmentioning

confidence: 99%

Triple‑negative breast cancer and its?association with obesity (Review)

Zou

Chen

et al. 2017

mol clin onc

View full text Add to dashboard Cite

show abstract

“…19,20 It has also been found that the blood glucose level is an important factor in breast cancer cell proliferation. 21,22 Our results show that the cell proliferation and mobility were increased when the glucose concentration in culture media was shifted from euglycemic to hyperglycemic levels.…”

Section: Discussionmentioning

confidence: 70%

Hyperglycemic tumor microenvironment induces perineural invasion in pancreatic cancer

Ma²,

Han

et al. 2015

Cancer Biology & Therapy

View full text Add to dashboard Cite

Glucose intolerance and frank diabetes mellitus (DM) can increase the risk of cancer death for pancreatic cancer (PanCa). However, the mechanism by which these factors influence cancer deaths is not clear. In this study, we established a model system to mimic the pancreatic tumor microenvironment in patients with DM to examine the biological behavior of PanCa cells and nerves in cell culture and in animals. Our in vitro studies demonstrated that hyperglycemia promoted the proliferation and invasion of PanCa cell lines and upregulated the expression of nerve growth factor in these cells. Also, the migration of Schwann cells (SCs) was inhibited by hyperglycemia and neurites exerted pathological regeneration. Furthermore, the interaction between the PanCa cells and nerves was enhanced in the tumor microenvironment. We further showed that hyperglycemia promoted the perineural invasion (PNI) of PanCa in vivo. These data suggest that DM worsens the prognosis of PanCa because of aggravated PNI. Thus, our study illustrates a novel mechanism by which hyperglycemia decreases survival in patients with PanCa.

show abstract

“…A higher level of ObRl was observed in ERα-positive MCF-7 and T47D breast cancer cells than in ERα-negative MDA-MB-231 and MDA-MB-435 breast cell lines (Garofalo et al, 2004). Studies also indicate up-regulation of leptin-induced DNA synthesis and cell growth, mediated through various signaling pathways including the JAK/STAT, ERK1/2 and PKC-α pathways, in ERα-positive breast cancer cell lines Hu et al, 2002;Laud et al, 2002;Okumura et al, 2002;Catalano et al, 2003;Somasundar et al, 2003;Garofalo et al, 2004;Yin et al, 2004). Interestingly, not only leptin-induced cell growth but also leptin-stimulated cell transformation (anchorage-independent growth) is observed in ERα-positive T47D breast cancer cells, but not in normal breast epithelial cells (Hu et al, 2002).…”

Section: Breast Cancermentioning

confidence: 97%

“…Immunohistochemistry has demonstrated expression of leptin and ObR in normal and cancer mammary epithelium (Ishikawa et al, 2004), however, several studies have shown an involvement of leptin in mammary carcinogenesis (O'Brien et al, 1999;Dieudonne et al, 2002;Hu et al, 2002;Laud et al, 2002;Okumura et al, 2002;Cleary et al, 2003). A distinct over-expression of both leptin and ObR was shown in cancer tissue relative to non-cancer epithelium (Ishikawa et al, 2004).…”

Section: Leptin Receptormentioning

confidence: 99%

“…Garofalo et al (2004) showed that leptin stimulates the Akt/GSK3 survival pathway in breast cancer cells, and affects of leptin on cell cycle have been reported in breast cancer cells. Leptin induces cell cycle progression through enhancement of cdk2 and cyclin D1 levels (Okumura et al, 2002), and inactivates a cell cycle inhibitor, pRb, by hyperphosphorylating that protein (Garofalo et al, 2004). The mitogenic effects of leptin and leptin-dependent activation of STAT3 require steroid receptor coactivator (SRC-1), a member of the p160 family of steroid receptor modulators (Yin et al, 2004).…”

Section: Breast Cancermentioning

confidence: 99%

See 1 more Smart Citation

Roles of Leptin in Cancer Progression

Kang¹,

Moon

2010

Biomolecules and Therapeutics

View full text Add to dashboard Cite

-Growing evidence suggests a prominent role for leptin in human cancer progression. The intricate pattern of leptin cross-talk with other associated signaling pathways is a critical area of research that will ultimately contribute to comprehending the role of leptin in cancer progression. This review summarizes a portion of the current understanding of leptin signaling, with a critical focus on its contribution to tumor cell invasion and metastasis. Five topics are addressed in this review: (1) Leptin receptor, (2) Leptin signaling, (3) Leptin and cancer, and (4) Leptin and tumor invasion. Due to the complex cellular effects of leptin, a more precise understanding of leptin signaling pathways must still be elucidated. Leptin is clearly a major factor for stimulating tumor progression through a complex spectrum of interplay and cross-talk among various signaling molecules. An understanding of the role of leptin in invasion and metastasis will provide valuable information for establishing strategies to modulate leptin signaling, which should be a high priority for the development of anti-cancer therapeutics.

show abstract

Leptin and high glucose stimulate cell proliferation in MCF-7 human breast cancer cells: reciprocal involvement of PKC-α and PPAR expression

Cited by 192 publications

References 37 publications

Triple‑negative breast cancer and its?association with obesity (Review)

Triple‑negative breast cancer and its?association with obesity (Review)

Hyperglycemic tumor microenvironment induces perineural invasion in pancreatic cancer

Roles of Leptin in Cancer Progression

Contact Info

Product

Resources

About