Leptin stimulates migration and invasion and maintains cancer stem‑like properties in gastric cancer cells

• DOI: 10.3892/or.2022.8377
• Publication Date: 2022-07-21T09:01:26Z
• Authors: Ki Park; Eun Kim; Hyungmin Chin; Dong Yoon; Kyong-Hwa Jun
• Keywords: Leptin; Mitogen-Activated Protein Kinase Kinases; Vascular Endothelial Growth Factor A; 2. Zero hunger; Epithelial-Mesenchymal Transition; Articles; 3. Good health; 03 medical and health sciences; 0302 clinical medicine; Cell Movement; Stomach Neoplasms; Cell Line, Tumor; Neoplastic Stem Cells; Humans; Obesity; Cell Proliferation

Obesity is a risk factor for various types of cancer. Leptin, an adipocyte‑derived hormone, may stimulate the proliferation gastric cancer cells. However, effect leptin and underlying mechanism in remain unclear. In present study, role was evaluated. The on JAK‑STAT MEK signaling pathways investigated cells using wound‑healing cell invasion assays, immunoblotting inhibition studies. Cancer‑initiating derived from were used to investigate maintenance stemness epithelial‑mesenchymal transition (EMT) by immunoblotting. Clinicopathological characteristics including serum level overall survival (OS) analyzed patients with (n=23) without obesity. Leptin induced migration activating AKT ERK upregulating vascular endothelial growth (VEGF). increased mRNA protein levels markers (CD44) EMT (Snail N‑cadherin). Pharmacological inhibitors decreased leptin‑induced invasion, expression VEGF. associated elevated body mass index positively correlated (P=0.001 both). 5‑year OS rate not significantly different between two groups (P=0.098). stimulates pathways, contributes metastatic potential. findings support adverse obesity Consequently, targeting leptin‑associated have therapeutic potential