The pursuit of oncotargets through understanding defective cell regulation

Qiao, Meng; Shi, Qian; Pardee, Arthur B.

doi:10.18632/oncotarget.189

Cited by 6 publications

(1 citation statement)

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“…In closing, this article has aimed at viewing the cancer hallmark of sustained proliferative signalling from the point of the cell cycle and disruption of some basic control mechanisms (279)(280)(281)(282)(283)(284)(285)(286). Different pathways have been scrutinized, and the action of a number of potential and known environmental carcinogens discussed with respect to their action on specific routes committing cells to an indefinite proliferative span.…”

Section: Final Remarksmentioning

confidence: 99%

The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling

Engström

Darbre

Eriksson

et al. 2015

CARCIN

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The aim of this work is to review current knowledge relating the established cancer hallmark, sustained cell proliferation to the existence of chemicals present as low dose mixtures in the environment. Normal cell proliferation is under tight control, i.e. cells respond to a signal to proliferate, and although most cells continue to proliferate into adult life, the multiplication ceases once the stimulatory signal disappears or if the cells are exposed to growth inhibitory signals. Under such circumstances, normal cells remain quiescent until they are stimulated to resume further proliferation. In contrast, tumour cells are unable to halt proliferation, either when subjected to growth inhibitory signals or in the absence of growth stimulatory signals. Environmental chemicals with carcinogenic potential may cause sustained cell proliferation by interfering with some cell proliferation control mechanisms committing cells to an indefinite proliferative span.

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Section: Final Remarksmentioning

confidence: 99%

The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling

Engström

Darbre

Eriksson

et al. 2015

CARCIN

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FOXM1 (Forkhead box M1) in Tumorigenesis

Wierstra¹

2013

Advances in Cancer Research

156

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FOXM1 (Forkhead box M1) is a typical proliferation-associated transcription factor and is also intimately involved in tumorigenesis. FOXM1 stimulates cell proliferation and cell cycle progression by promoting the entry into S-phase and M-phase. Additionally, FOXM1 is required for proper execution of mitosis. In accordance with its role in stimulation of cell proliferation, FOXM1 exhibits a proliferation-specific expression pattern and its expression is regulated by proliferation and anti-proliferation signals as well as by proto-oncoproteins and tumor suppressors. Since these factors are often mutated, overexpressed, or lost in human cancer, the normal control of the foxm1 expression by them provides the basis for deregulated FOXM1 expression in tumors. Accordingly, FOXM1 is overexpressed in many types of human cancer. FOXM1 is intimately involved in tumorigenesis, because it contributes to oncogenic transformation and participates in tumor initiation, growth, and progression, including positive effects on angiogenesis, migration, invasion, epithelial-mesenchymal transition, metastasis, recruitment of tumor-associated macrophages, tumor-associated lung inflammation, self-renewal capacity of cancer cells, prevention of premature cellular senescence, and chemotherapeutic drug resistance. However, in the context of urethane-induced lung tumorigenesis, FOXM1 has an unexpected tumor suppressor role in endothelial cells because it limits pulmonary inflammation and canonical Wnt signaling in epithelial lung cells, thereby restricting carcinogenesis. Accordingly, FOXM1 plays a role in homologous recombination repair of DNA double-strand breaks and maintenance of genomic stability, that is, prevention of polyploidy and aneuploidy. The implication of FOXM1 in tumorigenesis makes it an attractive target for anticancer therapy, and several antitumor drugs have been reported to decrease FOXM1 expression.

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