Table 1 Leptin / Leptin Receptor mediated effects in Ovarian Cancer
From: Oncogenic role of dysregulated leptin signaling in the pathogenesis of ovarian cancer
| Leptin/Leptin Receptor expression or their action | Model/System | Mechanism of Action | Reference |
|---|---|---|---|
| Leptin mediated Effects | OVCAR-3 | Leptin inhibits caspase-3 expression and activity by modulating STAT3 and ERK1/2 signaling pathways in OVCAR-3 cells. | [74] |
| Leptin mediated Effects | OVCAR-3 and SKOV-3 | Leptin stimulates cell migration via MMP-9 expression and activity in OVCAR-3 but not SKOV-3 | [44] |
| Leptin mediated Effects | 17β-estradiol displayed antagonistic effect on leptin-induced cell migration and MMP-9 expression and activity | [76] | |
| Leptin mediated Effects | OC cells | Leptin induces EMT via PI3K/Akt/mTOR pathway activation. Inhibiting PI3K/Akt/mTOR impaired leptin-induced malignant transformation | |
| Leptin mediated Effects | Blocking Leptin inhibited peritoneal dissemination and suppressed ovarian malignant ascites-induced metastatic aggravation | ||
| Leptin mediated Effects | OVCAR3, SKOV3 and CaoV-3 | Leptin induced cell invasion via up-regulating uPA. Ob-Rb, RhoA/ROCK, PI3K/AKT, JAK/STAT pathways and NF-kB activation were involved in leptin-induced uPA expression | [50] |
| Leptin Receptor Expression | 35 Ovarian Cancer Patients | Endometrial neoplasms and long leptin isoform receptor expression were associated with an increased BMI. A role of long isoform in endometrial carcinogenesis is proposed. | [68] |
| Leptin mediated effects | OCCAR-3 | Leptin upregulates the expression of cyclin D1 and Mcl-1 to stimulate cell growth by activating the PI3K/AKT and MEK/ERK1/2 pathways in ovarian cancer. | [45] |
| Leptin expression | BG-1, OVCAR-3, and SKOV-3 | Both short and long isoforms of leptin receptors are expressed in IOSE-80PC (a post-crisis line), cells. In addition, treatment with leptin resulted in the growth stimulation of BG-1 cells, an activation of ERK1/2 and inhibition of constitutive phosphorylation of p38 MAPK | [58] |
| Leptin expression & Its Effects | OC cells | Leptin was highly expressed, promoting cell migration, invasion and proliferation, resulting in poor survival | [76] |
| Leptin level | 52 OC patients vs 50 control group with benign disease | Decreased leptin levels compared to control group (7.09 vs. 15.4 ng/mL), associated with risk of developing OC | [59] |
| Serum Leptin | 167 endometrial cancer cases | Elevated leptin levels showed a positive association with endometrium cancer | [61] |
| Leptin mediated action | SKOV3 and A2780 cells | Cross-talk between leptin and microRNA-182 and microRNA-96 affects the transformation and proliferation of ovarian cancer cells. | [69] |
| Serum Leptin | 30 patients with endometrial cancer | Leptin did not show any significant correlation with stage, grade, histological type and node metastases in endometrial cancer. | [77] |
| Leptin Receptor expression and leptin mediated action | 156 EOC samples and EOC cell lines. | Ob-R overexpression (59.2%) in EOC samples was significantly associated with poor progression free survival. Leptin promotes cell proliferation via activation of PI3-kinase/AKT signaling. | [15] |
| Serum and ascite samples | 70 OC patients | [18] | |
| Higher leptin and Ob-Rb levels, resulting in poor survival, higher leptin in overweight patient serum and ascite samples | |||
| Leptin Receptor Expression | Ob-Rb expression levels higher in ascites and metastases compared to primary tumors. | ||
| Leptin mediated action | Leptin increased cell migration and invasion via JAK-STAT3, PI3K/AKT, and RhoA/ROCK, maintained stem-like properties and mesenchymal phenotype, explaining poor survival outcome |