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Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

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Feitelson, Mark A., Arzumanyan, Alla, Kulathinal, Rob J., Blain, Stacy W., Holcombe, Randall F., Mahajna, Jamal, Marino, Maria, Martinez-Chantar, Maria L., Nawroth, Roman, Sanchez-Garcia, Isidro, Sharma, Dipali, Saxena, Neeraj K., Singh, Neetu, Vlachostergios, Panagiotis J., Guo, Shanchun, Honoki, Kanya, Fujii, Hiromasa, Georgakilas, Alexandros G., Bilsland, Alan, Amedei, Amedeo, Niccolai, Elena, Amin, Amr, Ashraf, S. Salman, Boosani, Chandra S., Guha, Gunjan, Ciriolo, Maria Rosa, Aquilano, Katia, Chen, Sophie, Mohammed, Sulma I., Azmi, Asfar S., Bhakta, Dipita, Halicka, Dorota, Keith, W. Nicol, Nowsheen, Somaira·2015·Seminars in Cancer Biology
DOI 10.1016/j.semcancer.2015.02.006
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Abstract

Proliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). These data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression.

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Metadata

Authors
Feitelson, M. A., Arzumanyan, A., Kulathinal, R. J., Blain, S. W., Holcombe, R. F., Mahajna, J., Marino, M., Martinez-Chantar, M. L., Nawroth, R., Sanchez-Garcia, I., Sharma, D., Saxena, N. K., Singh, N., Vlachostergios, P. J., Guo, S., Honoki, K., Fujii, H., Georgakilas, A. G., Bilsland, A., Amedei, A., Niccolai, E., Amin, A., Ashraf, S. S., Boosani, C. S., Guha, G., Ciriolo, M. R., Aquilano, K., Chen, S., Mohammed, S. I., Azmi, A. S., Bhakta, D., Halicka, D., Keith, W. N., & Nowsheen, S.
Venue
Seminars in Cancer Biology
Publisher
Elsevier BV
Published
2015-12
Volume
35
Pages
S25-S54
ISSN
1044-579X (ISSN-L)
DOI
10.1016/j.semcancer.2015.02.006
OpenAlex
W2026982091
Cited by
778
References
47
FWCI
10.66
Type
journal article
Language
en
Open access
hybrid
Licence
Funders
  • European Commission (MC-CIG-303514)
  • Associazione Italiana per la Ricerca sul Cancro (IG15221, 10636)
  • National Institutes of Health (AI076535)
  • University of Glasgow
  • National Science Foundation
  • Purdue University Center for Cancer Research
  • Avon Foundation for Women
  • Cancer Research UK (C301/A14762)
  • Ministero dell’Istruzione, dell’Università e della Ricerca (20125S38FA_002)
  • European Cooperation in Science and Technology (CM1201)
  • Ministero della Salute (GR-2011-02348047)
  • Breast Cancer Research Foundation (K01DK077137, 90047965, R03DK089130, SR/FT/LS-063/2008)
  • Seventh Framework Programme (CA155686, R01CA131294)
  • Al Jalila Foundation (AJF201454)
  • Ministry of Education, Culture, Sports, Science and Technology (24590493)
  • European Regional Development Fund
  • Ministerio de Ciencia e Innovación (SAF2012-32810, R01 CA109335-04A1)
  • Università degli Studi Roma Tre (CLA 2013)
  • Consejería de Educación, Junta de Castilla y León (BIO/SA06/13, FP7-ENV-2011)
  • American Cancer Society
  • Temple University
  • Terry Fox Foundation (TF-36)

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CoChat. (2026). Citation check: Sustained proliferation in cancer: Mechanisms and novel therapeutic targets. https://app.cochat.ai/papers/10.1016/j.semcancer.2015.02.006
The paper
Feitelson, M. A., Arzumanyan, A., Kulathinal, R. J., Blain, S. W., Holcombe, R. F., Mahajna, J., Marino, M., Martinez-Chantar, M. L., Nawroth, R., Sanchez-Garcia, I., Sharma, D., Saxena, N. K., Singh, N., Vlachostergios, P. J., Guo, S., Honoki, K., Fujii, H., Georgakilas, A. G., Bilsland, A., . . . Nowsheen, S. (2015). Sustained proliferation in cancer: Mechanisms and novel therapeutic targets. Seminars in Cancer Biology. https://doi.org/10.1016/j.semcancer.2015.02.006

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