ABSTRACT
Tumor cell energy metabolism is dependent on glycolysis and oxidative phosphorylation.Tumor cells,because of its rapid growth,often show increased intake of glucose and other nutrients,increased glycolysis and so on.In recent years,the study on energy metabolism of tumor cells has received extensive attention.This paper summarizes the required nutrients,regulatory networks and therapeutic targets in the energy metabolism of tumor cells,and provides important reference for future research and clinical treatment.
ABSTRACT
<p><b>OBJECTIVE</b>To observe the effects of rukangyin (RKY) on the lymphangiogenesis and lymph node metastasis of breast cancer transplantation tumor mice, thus exploring its anti-tumor metastasis mechanisms.</p><p><b>METHODS</b>Human breast cancer cell line MDA-MB-435S were in situ implanted into the mammary fat pad of 30 female nude mice to establish breast cancer transplantation tumor spontaneous metastasis model. They were randomly divided into six groups, i.e., the model control group, the 5-FU control group, the small, medium, large dose RKY groups, and the medium dose RKY +5-FU group, 5 in each. Normal saline was given to mice in the model control group at the daily dose of 0.4 mL/kg by gastrogavage. 5-FU was given to mice in the 5-FU control group at the daily dose of 30 mg/kg by peritoneal injection. RKY was given to mice in the small, medium, large dose RKY groups at the daily dose of 18, 45, and 90 g/kg by gastrogavage. 5-FU 30 mg/kg (by peritoneal injection) + RKY 45 g/( kg x d) (by gastrogavage) was given to mice in the medium dose RKY +5-FU group. All medication was carried out once daily for 6 successive weeks. The tumor volume, the tumor inhibition ratio, and the inhibition ratio of axillary lymph node metastasis were detected after medication. The lymphatic microvessel density (LMVD) and expressions of vascular endothelial growth factor-C (VEGF-C) and vascular endothelial growth factor receptor-3 (VEGFR-3) of the breast cancer tissues were detected using immunohistochemical assay.</p><p><b>RESULTS</b>Compared with the model control group, the tumor volume was markedly reduced in the small, medium, large dose RKY groups, and the medium dose RKY +5-FU group, the expressions of VEGF-C and VEGFR-3 were significantly down-regulated and LMVD were obviously lowered, showing statistical difference (P < 0.05, P < 0.01). The inhibition rates of tumor and axillary lymph node metastasis were highest and the LMVD was the lowest in the medium dose RKY +5-FU group, showing statistical difference when compared with other medication groups (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>RKY might inhibit the lymph node metastasis of breast cancer possibly through intervening the expressions of VEGF-C and VEGFR-3, and suppressing lymphangiogenesis.</p>
Subject(s)
Animals , Female , Humans , Mice , Breast Neoplasms , Metabolism , Pathology , Cell Line, Tumor , Down-Regulation , Drugs, Chinese Herbal , Pharmacology , Lymphangiogenesis , Lymphatic Metastasis , Lymphatic Vessels , Mice, Inbred BALB C , Mice, Nude , Vascular Endothelial Growth Factor C , Metabolism , Vascular Endothelial Growth Factor Receptor-3 , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the changes of the potentials and structure of the guinea pig cochlear during whole cochlear perfusion with glutamate.</p><p><b>METHODS</b>Cochlear microphonics (CM), compound action potential (CAP), distortion product otoacoustic emission (DPOAE) and auditory brainstem response (ABR) were measured to indicate the cochlear functional properties during whole cochlear perfusion. The morphology of the cochlear was monitored by transmission electron microscopy.</p><p><b>RESULTS</b>There were no significant DPOAE changes before and after glutamate perfusion. CM I/O function maintained a nonlinear characteristic during infusion. After glutamate perfusion, ABR latencies were delayed. There was significant difference in CAP threshold before and after glutamate perfusion. The average CAP threshold was elevated 35 dB. The OHCs appeared normal, but IHCs and afferent dendrites showed cytoplasmic blebs after glutamate infusion.</p><p><b>CONCLUSIONS</b>Glutamate is thought to be a primary amino acid neurotransmitter at the synapses formed by cochlear hair cells and spiral ganglion neurons. However, the excessive glutamate is neurotoxic for cells, and it can destroy the IHCs and spiral ganglion neurons. The present method can also be built up as an animal model of auditory neuropathy.</p>