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A study of the Crabtree effect in Novikoff ascites-hepatoma cells.

ABSTRACT: Novikoff ascites-hepatoma cells show no Crabtree effect on the addition of glucose to tumour-cell suspensions, and convert a significant part of the added glucose into glycogen. Treatment of the cells with 2-deoxyglucose or glucose in the presence of iodoacetate inhibits respiration and decreases glycogen synthesis from glucose. Short-term experiments indicate a slight inhibition of glucose uptake for a brief period, due either to ATP accumulation in the mitochondria or to glucose 6-phosphate-mediated inhibition of hexokinase. Utilization of glucose metabolites and ATP for glycogen synthesis appears to remove inhibition of glucose uptake, and perhaps accounts for the absence of respiratory inhibition, by relieving a deficiency of ADP for the mitochondria. Decreased respiration in the presence of 2-deoxyglucose or glucose in the presence of iodoacetate could be due to the change in mitochondrial structure or permeability, caused by the significant loss of adenine nucleotides.

SUBMITTER: Nigam VN

PROVIDER: S-EPMC1265010 | biostudies-other | 1966 May

REPOSITORIES: biostudies-other

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Project description:Epirubicin is a chemotherapy agent for hepatocellular carcinoma (HCC). However, the outcome of HCC patients receiving epirubicin remains unsatisfactory. Moreover, our previous study indicated that celecoxib suppresses HCC progression and liver cancer stemness. This study evaluated the potential of celecoxib to serve as a complementary therapy during epirubicin treatment. Cell proliferation, apoptosis, invasiveness, and anchorage-independent growth were analyzed in hepatoma cells. Therapeutic efficacy was validated in rat orthotopic Novikoff hepatoma. After animal sacrifice, the antitumor mechanism of celecoxib and epirubicin combined therapy was investigated by histological analysis. Celecoxib enhanced the cytotoxic activity of epirubicin in HCC cells by promoting apoptosis. Besides, celecoxib potentiated the antineoplastic function of epirubicin in inhibiting the invasiveness and anchorage-independent growth of HCC cells. Ultrasound monitoring showed that combined therapy was more potent than either therapy alone in perturbing HCC progression. Consistently, the size and weight of dissected HCC tissues from rats receiving combined therapy were smallest among all groups. HCC treated with combined therapy exhibited the highest prevalence of apoptotic cells, which was accompanied by reduced proliferating and angiogenic activities in tumor tissues. Moreover, the expression levels of cancer stemness markers (CD44 and CD133) and drug transporter MDR-1 were significantly diminished in rats receiving combined therapy. Besides, celecoxib treatment increased the infiltration of cytotoxic T lymphocytes (CTLs) and reduced the number of regulatory T cells (Tregs), tumor-associated macrophages (TAMs), and the expression of immune checkpoint PD-L1 in HCC tissues during epirubicin therapy. Celecoxib augmented the therapeutic efficacy while modulated cancer stemness and antitumor immunity. Thus, celecoxib may serve as complementary therapy to improve the outcome of patients with advanced HCC during epirubicin treatment.

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A study of the Crabtree effect in Novikoff ascites-hepatoma cells.

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