Antiproliferative and Apoptotic Effects of Iron Chelators on Human Cervical Carcinoma Cells

Simonart, Thierry; Boelaert, Johan R.; Mosselmans, Roger; Andrei, Gracíela; Noël, Jean Christophe; Clercq, Erik De; Snoeck, Robert

doi:10.1006/gyno.2001.6570

Cited by 62 publications

(37 citation statements)

References 27 publications

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“…Interestingly, there were marked differences in studies conducted with iron chelators in vivo compared with those performed in vitro. Treatment with DFO for 4 wk did not inhibit the xenograft growth of human neuroblastoma or cervical carcinoma cell lines (27) in nude mice (24) although growth of the cervical carcinoma cell lines was inhibited by DFO in vitro (29). The possible involvement of nonamidated gastrins in the above effects will be worthy of future investigation, as 80% of neuroblastomas have been shown to express gastrin mRNA, whereas expression of the mRNA encoding the CCK 2 R, which is specific for amidated gastrins, was limited to 10% of the same tumors (23).…”

Section: Discussionmentioning

confidence: 99%

Stimulation of proliferation in the colorectal mucosa by gastrin precursors is blocked by desferrioxamine

Ferrand

Lachal

Bramante

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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Precursors of the peptide hormone gastrin stimulate proliferation in the colorectal mucosa and promote the development of colorectal carcinoma. Gastrins bind two ferric ions selectively and with high affinity, and the biological activity of glycine-extended gastrin (Ggly) in vitro is dependent on the presence of ferric ions. The aim of the present study was to determine whether or not iron is required for biological activity of progastrin and Ggly in vivo. Rats that had undergone a colostomy were infused with Ggly, and proliferation was measured in the defunctioned rectal mucosa. Proliferation was also measured in the colonic mucosa of hGAS and MTI-Ggly mice, which, by definition, overexpress progastrin and Ggly, respectively. The requirement for iron was assessed by thrice-weekly injection of the chelating agent desferrioxamine (DFO). The proliferation index in the defunctioned rectal mucosa was significantly increased in the Ggly-infused rats, and the increase was significantly reduced after treatment with DFO. Treatment with DFO significantly reduced the crypt height and proliferation index in the colonic mucosa of hGAS and MTI-Ggly mice but had no effect on the same variables in wild-type mice. These observations are consistent with the hypothesis that the biological activity of progastrin and Ggly in vivo is dependent on the presence of ferric ions and further suggest that chelating agents may block the stimulatory effects of gastrin precursors in the development of colorectal carcinoma.

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Section: Discussionmentioning

confidence: 99%

Stimulation of proliferation in the colorectal mucosa by gastrin precursors is blocked by desferrioxamine

Ferrand

Lachal

Bramante

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…For instance, DFO has been demonstrated to induce apoptosis in a number of cancer cell lines including ovarian cancer, 202 neuroblastoma, 203 Kaposi's sarcoma, 122 malignant oral keratinocytes 169 and cervical carcinomas. 204 Other chelators, including Triapine, 205 311, 90 Tachpyridine, 132,206,207 O-Trensox 208 and Dp44mT 93 have also been shown to induce apoptosis in a variety of neoplastic cell types both in vitro and in vivo.…”

Section: The Molecular Targets Of Iron Chelators and Their Effects Onmentioning

confidence: 99%

Tuning Cell Cycle Regulation with an Iron Key

Yu¹,

Kovačević²,

Richardson³

2007

Cell Cycle

217

190

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“…Hemin caused accumulation of hemoglobin in K562 cells and diminished growth potential of the cells [35][36][37]. On the other hand, DFO has also been shown to have antiproliferative effects on a number of cell lines in vitro, including various carcinomas, hepatoma, leukemia, and neuroblastoma cells [21][22][23][24][25][26]. We have also demonstrated that DFO and hemin treatment caused the inhibition of K562 cell proliferation.…”

Section: Discussionmentioning

confidence: 89%

“…Iron chelation by DFO has been shown to inhibit the growth of and/or to induce apoptosis in malignant leukemia, neuroblastoma, melanoma, heaptoma, Kaposi's sarcoma, and cervical cancer cell lines [20][21][22][23][24][25][26][27]. When present in excess within the cell, iron can be toxic due to its ability to catalyze the formation of damaging radicals, which promote cellular injury and cell death [28] Also, it is well known that iron deficiency leads to different types of anemia.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Hemin and Deferoxamine on Selenium, Zinc, and Iron Levels of K562 Cells

Küçükkaya¹,

Afrasyap²

2011

JCT

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No differences were observed in selenium levels of the control group compared with the hemin-induced group. Also there were no significant differences observed in the zinc levels of control cells compared with deferoxamine-and hemin-induced cells. Iron levels of hemin-induced cells were decreased on the fourth day compared with the third day. On the third day, iron levels of hemin-induced cells were significantly increased compared to the control group. Our observations suggest that alterations of selenium and zinc levels may play a role in hemin-inductionand deferoxamine-inhibition, respectively. On the other hand, iron levels may influence both in hemin-induction and deferoxamine-inhibition of K562 human leukemia cell line.

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Antiproliferative and Apoptotic Effects of Iron Chelators on Human Cervical Carcinoma Cells

Cited by 62 publications

References 27 publications

Stimulation of proliferation in the colorectal mucosa by gastrin precursors is blocked by desferrioxamine

Stimulation of proliferation in the colorectal mucosa by gastrin precursors is blocked by desferrioxamine

Tuning Cell Cycle Regulation with an Iron Key

The Effect of Hemin and Deferoxamine on Selenium, Zinc, and Iron Levels of K562 Cells

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