Serotonin transporter mRNA expression in the dorsal raphe nucleus of a tumor bearing mouse

Jahng, Jeong Won; Choi, Si Ho; Joo, Mi Kyoung; Kim, Nam Youl; Hwang, Soon Jeong; Lee, Jong-Ho

doi:10.1038/emm.2005.9

Cited by 12 publications

(4 citation statements)

References 24 publications

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“…14,16 Significant reduction in leptin levels in OSCC patients was previously observed, and it was correlated with weight loss and cachexia status, 15,16,19 but there are controversies about this fact in the literature. 21 Our results suggested a possible involvement of serum leptin as well tissue protein expression and LepR mRNA in OSCC. We believe that leptin can act not only by endocrine actions but also by an autocrine pathway.…”

Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

“…Studies have focused on the investigation of leptin plasma levels [14][15][16] and gene polymorphisms of Lep or its receptor, LepR, 17,18 associating the findings with development and progression risk of OSCC. [14][15][16][17][18][19][20][21] However, there is no investigation focusing on functional effect and molecular changes caused by Lep and LepR in OSCC. Thus, we hypothesized that Lep could favor phenotypic behavior of human oral cancer cells lines.…”

Section: Introductionmentioning

confidence: 99%

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Leptin acts on neoplastic behavior and expression levels of genes related to hypoxia, angiogenesis, and invasiveness in oral squamous cell carcinoma

et al. 2017

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Leptin, one of the main hormones controlling energy homeostasis, has been associated with different cancer types. In oral cancer, its effect is not well understood. We investigated, through in vitro and in vivo assays, whether leptin can affect the neoplastic behavior of oral squamous cell carcinoma. Expression of genes possibly linked to the leptin pathway was assessed in leptin-treated oral squamous cell carcinoma cells and also in tissue samples of oral squamous cell carcinoma and oral mucosa, including leptin, leptin receptor, hypoxia-inducible factor 1-alpha, E-cadherin, matrix metalloproteinase-2, matrix metalloproteinase-9, Col1A1, Ki67, and mir-210. Leptin treatment favored higher rates of cell proliferation and migration, and reduced apoptosis. Accordingly, leptin-treated oral squamous cell carcinoma cells show decreased messenger RNA caspase-3 expression, and increased levels of E-cadherin, Col1A1, matrix metalloproteinase-2, matrix metalloproteinase-9, and mir-210. In tissue samples, hypoxia-inducible factor 1-alpha messenger RNA and protein expression of leptin and leptin receptor were high in oral squamous cell carcinoma cases. Serum leptin levels were increased in first clinical stages of the disease. In animal model, oral squamous cell carcinoma-induced mice show higher leptin receptor expression, and serum leptin level was increased in dysplasia group. Our findings suggest that leptin seems to exert an effect on oral squamous cell carcinoma cells behavior and also on molecular markers related to cell proliferation, migration, and tumor angiogenesis.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Leptin acts on neoplastic behavior and expression levels of genes related to hypoxia, angiogenesis, and invasiveness in oral squamous cell carcinoma

et al. 2017

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“…The involvement of brain stem GABAergic neurotransmission in the regulation of the hepatic proliferation through the sympathetic stimulation was reported from our laboratory [16]. Oral carcinoma suppressed the expression of 5-HT transporter in the dorsal raphe nucleus [17] elucidating the CNS serotonergic alteration during neoplasia.…”

Section: Introductionmentioning

confidence: 91%

Increased 5-HT2C receptor binding in the brain stem and cerebral cortex during liver regeneration and hepatic neoplasia in rats

Sulaiman

Joseph

Paulose

2007

Journal of the Neurological Sciences

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In the present study, serotonin 2C (5-HT(2C)) receptor binding parameters in the brainstem and cerebral cortex were investigated during liver generation after partial hepatectomy (PH) and N-nitrosodiethylamine (NDEA) induced hepatic neoplasia in male Wistar rats. The serotonin content increased significantly (p<0.01) in the cerebral cortex after PH and in NDEA induced hepatic neoplasia. Brain stem serotonin content increased significantly (p<0.05) after PH and (p<0.001) in NDEA induced hepatic neoplasia. The number and affinity of the 5-HT(2C) receptors in the crude synaptic membrane preparations of the brain stem showed a significant (p<0.001) increase after PH and in NDEA induced hepatic neoplasia. The number and affinity of 5-HT(2C) receptors increased significantly (p<0.001) in NDEA induced hepatic neoplasia in the crude synaptic membrane preparations of the cerebral cortex. There was a significant (p<0.01) increase in plasma norepinephrine in PH and (p<0.001) in NDEA induced hepatic neoplasia, indicating sympathetic stimulation. Thus, our results suggest that during active hepatocyte proliferation 5-HT(2C) receptor in the brain stem and cerebral cortex are up-regulated which in turn induce hepatocyte proliferation mediated through sympathetic stimulation.

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Head and neck squamous cell carcinoma cell lines: Established models and rationale for selection

et al. 2006

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Serotonin transporter mRNA expression in the dorsal raphe nucleus of a tumor bearing mouse

Cited by 12 publications

References 24 publications

Leptin acts on neoplastic behavior and expression levels of genes related to hypoxia, angiogenesis, and invasiveness in oral squamous cell carcinoma

Leptin acts on neoplastic behavior and expression levels of genes related to hypoxia, angiogenesis, and invasiveness in oral squamous cell carcinoma

Increased 5-HT2C receptor binding in the brain stem and cerebral cortex during liver regeneration and hepatic neoplasia in rats

Head and neck squamous cell carcinoma cell lines: Established models and rationale for selection

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