Fig. 5.

Elevated OB-R expression in human HCC and correspondence of OB-R and OCT4 in multiple tumor types. (A) Immunohistochemical analysis of HCC tumors. Surgically resected HCC patient tumor specimens from age-matched specimens were fixed and stained with antisera to CD133 and OB-R and counterstained with DAPI to indicate nuclei. White arrows indicate examples of cells strongly coexpressing CD133 and OB-R. (Scale bar, 100 μm.) (B) Quantification of CD133 and OB-R reactivity. CD133⁺ and CD133⁻ cells were scored for the degree of OB-R immunopositivity. Brackets indicate statistically significant (**P < 0.01) comparisons between groups. (C) Immunoblot analysis of lysates prepared from surgically resected HCC patient specimens (T) and matched normal tissue (N). Immunoblot of actin serves as a control for protein loading. (D) Scatter plots showing results from meta-analysis comparing the expression levels of OB-R and OCT4 across multiple tumor samples. Expression data were collected from pancreatic and breast cancers, multiple myeloma, and CaCo-2 colon adenocarcinoma cells. (E) Model of leptin action on TISCs in promoting tumor growth. Leptin signaling triggers phosphorylation and activation of STAT3 to induce OCT4 and SOX2, thereby completing a self-reinforcing oncogenic signaling circuit in TISCs. Cytokines such as IL-6 and TNF may also contribute to this signaling network.