Mechanism of growth inhibitory effect of Mitomycin-C on cultured human retinal pigment epithelial cells: Apoptosis and cell cycle arrest

Kang, Seok Seon; Chung, Hum; Yoo, Young; Lee, Jun Gyo; Choi, Young In; Yu, Young Suk

doi:10.1076/ceyr.22.3.174.5513

Cited by 53 publications

(45 citation statements)

References 17 publications

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“…We induced cell-cycle arrest of glioma TSCs in M phase with mitomycin C (MMC; ref. 32) and evaluated glycolysis in these cells ( Supplementary Fig. S4A).…”

Section: Pdgf Regulation Of Glycolysis In Tscs Is Independent Of Its mentioning

confidence: 99%

Proliferation-Independent Control of Tumor Glycolysis by PDGFR-Mediated AKT Activation

Ran¹,

Liu²,

Hitoshi³

et al. 2013

Cancer Research

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The differences in glucose metabolism that distinguish most malignant and normal tissues have called attention to the importance of understanding the molecular mechanisms by which tumor energy metabolism is regulated. Receptor tyrosine kinase (RTK) pathways that are implicated in proliferation and transformation have been linked to several aspects of tumor glucose metabolism. However, the regulation of glycolysis has invariably been examined under conditions in which proliferation is concomitantly altered. To determine whether RTKs directly regulate glycolysis without prerequisite growth modulation, we first identified a specific RTK signaling pathway, platelet-derived growth factor (PDGF)/PDGF receptor (PDGFR) that regulates glycolysis in glioma-derived tumor stem-like cells from a novel mouse model. We determined that PDGFregulated glycolysis occurs independent of PDGF-regulated proliferation but requires the activation of AKT, a known metabolic regulator in tumor. Our findings identifying a key characteristic of brain tumors, aerobic glycolysis, mediated by a pathway with multiple therapeutic targets suggests the possibility of inhibiting tumor energy metabolism while also treating with agents that target other pathways of pathologic significance.

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“…We induced cell-cycle arrest of glioma TSCs in M phase with mitomycin C (MMC; ref. 32) and evaluated glycolysis in these cells ( Supplementary Fig. S4A).…”

Section: Pdgf Regulation Of Glycolysis In Tscs Is Independent Of Its mentioning

confidence: 99%

Proliferation-Independent Control of Tumor Glycolysis by PDGFR-Mediated AKT Activation

Ran¹,

Liu²,

Hitoshi³

et al. 2013

Cancer Research

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“…Metabolically reactive mitomycin C induces DNA damage via DNA-alkylation, DNA-mono-adduct formation, and intrastrand cross-linking (8,9). Such reactions eventually result in antitumor effects in a broad range of human cancers (10)(11)(12)(13). Doxorubicin is another useful wide-spectrum anticancer drug with a mechanism of action distinct from that of mitomycin C (14).…”

Section: Introductionmentioning

confidence: 99%

Mitomycin C and doxorubicin elicit conflicting signals by causing accumulation of cyclin E prior to p21WAF1/CIP1 elevation in human hepatocellular carcinoma cells

Choi

Shen²,

Woo³

et al. 2011

Int J Oncol

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Abstract. Proteins involved in the G 1 phase of the cell cycle are aberrantly expressed, sometimes in mutated forms, in human cancers including human hepatocellular carcinoma. Upon attack by a DNA-damaging anticancer drug, a cell arrests at the G 1 phase; this is a safety feature prohibiting entry of DNA-damaged cells into S-phase. p21 WAF1/CIP1 prevents damaged cells from progressing to the next cell cycle. Here, we show that, in response to mitomycin C and doxorubicin, human hepatocellular carcinoma cells generate conflicting signals, mediated by cyclin E and p21 WAF1/CIP1

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“…8A) Ϫ/Ϫ embryos could result from a block in mitosis or a lengthening of the duration of the M phase. To discriminate between these two possibilities, E4.5 blastocysts were treated for 7 h with mitomycin C, an agent which cross-links adjacent guanines and so blocks cells in S or G 2 phases in response to the activation of the DNA damage checkpoint (19). As shown in Fig.…”

Section: Abnormal Mitosis In Omcg1 Mutant Embryos the Observation Thmentioning

confidence: 99%

Impaired Mitotic Progression and Preimplantation Lethality in Mice Lacking OMCG1, a New Evolutionarily Conserved Nuclear Protein

Artus

Vandormael-Pournin

Frödin

et al. 2005

Molecular and Cellular Biology

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While highly conserved through evolution, the cell cycle has been extensively modified to adapt to new developmental programs. Recently, analyses of mouse mutants revealed that several important cell cycle regulators are either dispensable for development or have a tissue-or cell-type-specific function, indicating that many aspects of cell cycle regulation during mammalian embryo development remain to be elucidated. Here, we report on the characterization of a new gene, Omcg1, which codes for a nuclear zinc finger protein. Embryos lacking Omcg1 die by the end of preimplantation development. In vitro cultured Omcg1-null blastocysts exhibit a dramatic reduction in the total cell number, a high mitotic index, and the presence of abnormal mitotic figures. Importantly, we found that Omcg1 disruption results in the lengthening of M phase rather than in a mitotic block. We show that the mitotic delay in Omcg1 ؊/؊ embryos is associated with neither a dysfunction of the spindle checkpoint nor abnormal global histone modifications. Taken together, these results suggest that Omcg1 is an important regulator of the cell cycle in the preimplantation embryo.

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Mechanism of growth inhibitory effect of Mitomycin-C on cultured human retinal pigment epithelial cells: Apoptosis and cell cycle arrest

Abstract: This study demonstrated that the response of RPE cells to MMC was bi-directional: 1) partial arrest of the cell cycle at S, G2/M phase, and 2) induction of apoptotic cell death.

Cited by 53 publications

References 17 publications

Proliferation-Independent Control of Tumor Glycolysis by PDGFR-Mediated AKT Activation

Proliferation-Independent Control of Tumor Glycolysis by PDGFR-Mediated AKT Activation

Mitomycin C and doxorubicin elicit conflicting signals by causing accumulation of cyclin E prior to p21WAF1/CIP1 elevation in human hepatocellular carcinoma cells

Impaired Mitotic Progression and Preimplantation Lethality in Mice Lacking OMCG1, a New Evolutionarily Conserved Nuclear Protein

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