Coordinating cell proliferation and differentiation

Zhu, Liang; Skoultchi, Arthur I.

doi:10.1016/s0959-437x(00)00162-3

Cited by 213 publications

(178 citation statements)

References 58 publications

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“…17, 41), which binds RARa, thereby trans-activating RA target genes. Previous reports have suggested that inhibition of ALDH1A1 activity leads to depletion of cellular RA, which, in most hematopoietic stem cells, delays the differentiation (42) by delaying exit from the cell-cycle exit (43) and fostering continued proliferation. Both ALDH activity and p-Akt were reduced significantly upon exposure to b-escin in lung tumor cells (Figs.…”

Section: Discussionmentioning

confidence: 99%

β-Escin Inhibits NNK-Induced Lung Adenocarcinoma and ALDH1A1 and RhoA/Rock Expression in A/J Mice and Growth of H460 Human Lung Cancer Cells

Patlolla

Biddick

et al. 2013

Cancer Prevention Research

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Lung cancer is the leading cause of cancer-related deaths. b-Escin, a triterpene saponin isolated from horse chestnut seeds, was tested for inhibition of lung adenoma and adenocarcinoma induced by the tobacco carcinogen 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in female A/J mice; and its possible mode of action was evaluated using the H460 human lung cancer cell line. At 6 weeks of age, 35 mice were fed AIN-76A-modified diet, and one week later, lung tumors were induced with a single intraperitoneal (i.p.) injection of 10 mmol NNK/mouse. Three weeks after the NNK treatment, groups of mice were fed either control or experimental diets containing 500 ppm for 20 weeks (10 control, 5 b-escin) or 36 weeks (15 control, 5 b-escin) and evaluated for lung tumor via histopathologic methods. Administration of 500 ppm b-escin significantly suppressed lung tumor (adenoma þ adenocarcinoma) formation by more than 40% (P < 0.0015) at 20 weeks and by 53.3% (P < 0.0001) at 37 weeks. b-Escin inhibited NNK-induced lung adenocarcinoma formation by 65% (P < 0.001) at 20 weeks and by 53% (P < 0.0001) at 37 weeks. Immunohistochemical analysis revealed that lung tumors from mice exposed to b-escin showed significantly reduced aldehyde dehydrogenase (ALDH)1A1 and phospho-Akt (p-Akt) expression when compared with those in mice fed control diet. Aldefluor assay for ALDH revealed that among H460 lung cancer cells treated with different concentrations of b-escin (0-40 mmol/L), the subpopulation of cells with elevated ALDH activity was inhibited significantly. Our findings suggest that b-escin inhibits tobacco carcinogeninduced lung tumor formation by modulating ALDH1A1-positive cells and RhoA/Rock signaling. Cancer Prev Res; 6(10);

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Section: Discussionmentioning

confidence: 99%

β-Escin Inhibits NNK-Induced Lung Adenocarcinoma and ALDH1A1 and RhoA/Rock Expression in A/J Mice and Growth of H460 Human Lung Cancer Cells

Patlolla

Biddick

et al. 2013

Cancer Prevention Research

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“…Thus, the arrest of cell cycle is the first event that occurs at the moment when the fate of the cells is decided to either differentiation or proliferation. Usually, the decision of cells to differentiate is made in the G0/G1 phase of the cell cycle, and the induction of differentiation is believed to follow G0/G1 cell cycle arrest (Zhu and Skoultchi, 2001). The regulation of cells entering from the G1 phase into S phase is particularly important, as the cells normally must pass through a restriction point in late G1 to progress to the S phase (Pardee, 1989).…”

Section: Involving In the Arrest Of Cell Cycle In Cancer Cellsmentioning

confidence: 99%

Progress on Understanding the Anticancer Mechanisms of Medicinal Mushroom: Inonotus Obliquus

Song¹,

Liu²,

Kong³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…It is known that cancer cell differentiation requires cell-cycle exit, by which at least two waves of signaling events are involved: induction of cell-cycle arrest and transition into transactivation of target genes that regulates differentiation (Studzinski and Harrison, 1999;Zhu and Skoultchi, 2001). As RAinduced cancer cell differentiation usually takes 3-7 days depending on the different cell types (Taneja et al, 1997;Wang et al, 2002Wang et al, , 2006Zhang et al, 2004), we assessed changes in gene expression from the induction of osteosarcoma cell-cycle G 1 arrest to differentiation induced by RA or S77A (Figures 1-3) in parallel.…”

Section: Raras77a Expression In U2os Cells Inhibits Osteosarcoma Formmentioning

confidence: 99%

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

et al. 2010

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Coordinating cell proliferation and differentiation

Cited by 213 publications

References 58 publications

β-Escin Inhibits NNK-Induced Lung Adenocarcinoma and ALDH1A1 and RhoA/Rock Expression in A/J Mice and Growth of H460 Human Lung Cancer Cells

β-Escin Inhibits NNK-Induced Lung Adenocarcinoma and ALDH1A1 and RhoA/Rock Expression in A/J Mice and Growth of H460 Human Lung Cancer Cells

Progress on Understanding the Anticancer Mechanisms of Medicinal Mushroom: Inonotus Obliquus

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

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