The rodent non-genotoxic hepatocarcinogen nafenopin suppresses apoptosis preferentially in non-cycling hepatocytes but also elevates CDK4, a cell cycle progression factor
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منابع مشابه
The non-genotoxic hepatocarcinogen nafenopin suppresses rodent hepatocyte apoptosis induced by TGFbeta1, DNA damage and Fas.
The suppression of apoptosis may contribute to the carcinogenicity of the peroxisome proliferators (PPs), a class of non-genotoxic rodent hepatocarcinogens. Our previous work demonstrated that the PP nafenopin suppressed both spontaneous and transforming growth factor beta1 (TGFbeta1)-induced hepatocyte apoptosis both in vivo and in vitro. Here, we extend these observations by demonstrating the...
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Suppression of apoptosis has been implicated as a mechanism for the hepatocarcinogenicity of the peroxisome proliferator class of non-genotoxic carcinogens. The ability of the peroxisome proliferator nafenopin to suppress or delay the onset of liver apoptosis was investigated using primary cultures of rat hepatocytes and the Reuber hepatoma cell line FaO. 50 microM nafenopin reversibly maintain...
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Cancer is characterized by abnormally excessive cell proliferation. Cell proliferation, the process by which a cell grows and divides to produce two daughter cells. Each of these daughter cells divides to produce two new cells, steps that are called cell cycle. Meanwhile, apoptosis is a highly regulated process of cell death, which is involved not only in the development of shape and morphogene...
متن کاملNafenopin causes protein kinase C-mediated serine phosphorylation and loss of function of connexin 32 protein in rat hepatocytes without aberrant expression or localization.
The characteristics and mechanism of the inhibition of connexin-mediated gap junctional communication by the non-genotoxic rodent hepatocarcinogen, nafenopin, has been studied in rat hepatocytes. Nafenopin caused a time- and concentration-dependent inhibition of dye coupling in hepatocytes as assessed by transfer of microinjected lucifer yellow. A half-maximum inhibitory effect of nafenopin occ...
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Renal cell carcinoma (RCC) is the major cause of kidney malignancy-related deaths. Rho GTPases are key regulators in cancer cell metastasis. ARHGAP24, a Rac-specific member of the Rho GTPase-activating protein family, acts as a functional target of cancer cell migration and invasion. In the present study, we identified ARHGAP24 expression is downregulated in renal cancer tissues and is highly c...
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ژورنال
عنوان ژورنال: Carcinogenesis
سال: 1998
ISSN: 1460-2180
DOI: 10.1093/carcin/19.10.1743