The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
Tumor cell survival pathways activated by photodynamic therapy: a molecular basis for pharmacological inhibition strategies
Open accessAbstract
Photodynamic therapy (PDT) has emerged as a promising alternative to conventional cancer therapies such as surgery, chemotherapy, and radiotherapy. PDT comprises the administration of a photosensitizer, its accumulation in tumor tissue, and subsequent irradiation of the photosensitizer-loaded tumor, leading to the localized photoproduction of reactive oxygen species (ROS). The resulting oxidative damage ultimately culminates in tumor cell death, vascular shutdown, induction of an antitumor immune response, and the consequent destruction of the tumor. However, the ROS produced by PDT also triggers a stress response that, as part of a cell survival mechanism, helps cancer cells to cope with the PDT-induced oxidative stress and cell damage. These survival pathways are mediated by the transcription factors activator protein 1 (AP-1), nuclear factor E2-related factor 2 (NRF2), hypoxia-inducible factor 1 (HIF-1), nuclear factor κB (NF-κB), and those that mediate the proteotoxic stress response. The survival pathways are believed to render some types of cancer recalcitrant to PDT and alter the tumor microenvironment in favor of tumor survival. In this review, the molecular mechanisms are elucidated that occur post-PDT to mediate cancer cell survival, on the basis of which pharmacological interventions are proposed. Specifically, pharmaceutical inhibitors of the molecular regulators of each survival pathway are addressed. The ultimate aim is to facilitate the development of adjuvant intervention strategies to improve PDT efficacy in recalcitrant solid tumors.
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1 retracted
RETRACTED: Acriflavine inhibits HIF-1 dimerization, tumor growth, and vascularization
Lee, K., Zhang, H., Qian, D. Z., Rey, S., Liu, J. O., & Semenza, G. L. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0909353106 · Cited by 451
RetractedTargeting HIF-1 for cancer therapy
Semenza, G. L. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1187 · Cited by 6,717 · cited 1×
“Intratumoral angiogenesis, endothelial cell proliferation, and matrix and vascular remodeling are modulated by HIF-1 via upregulation of VEGF, endothelin 1 (EDN1), plasminogen activator inhibitor 1 (PAI1, SERPINE1), (inducible) nitric oxide synthase 2 (NOS2), angiopoietin (ANGPT) 1 and 2, erythropoietin (EPO), and tra…”
BackgroundJaakkola, P., Mole, D. R., Tian, Y.-M., Wilson, M. I., Gielbert, J., Gaskell, S. J., Kriegsheim, A. V., Hebestreit, H. F., Mukherji, M., Schofield, C. J., et al. (2001) · Science · doi:10.1126/science.1059796 · Cited by 5,535
The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis
Maxwell, P. H., Wiesener, M. S., Chang, G.-W., Clifford, S. C., Vaux, E. C., Cockman, M. E., Wykoff, C. C., Pugh, C. W., Maher, E. R., & Ratcliffe, P. J. (1999) · Nature · doi:10.1038/20459 · Cited by 5,180
Hypoxia — a key regulatory factor in tumour growth
Harris, A. L. (2002) · Nature Reviews Cancer · doi:10.1038/nrc704 · Cited by 5,177
Matrix Metalloproteinases: Regulators of the Tumor Microenvironment
Kessenbrock, K., Plaks, V., & Werb, Z. (2010) · Cell · doi:10.1016/j.cell.2010.03.015 · Cited by 5,151
HIFα Targeted for VHL-Mediated Destruction by Proline Hydroxylation: Implications for O 2 Sensing
Ivan, M., Kondo, K., Yang, H., Kim, W., Valiando, J., Ohh, M., Salic, A., Asara, J. M., Lane, W. S., & Kaelin Jr., W. G. (2001) · Science · doi:10.1126/science.1059817 · Cited by 4,735 · cited 1×
“HIF-1 activation by hypoxia HIF-1α acts as an oxygen sensor in that it is constantly targeted for proteasomal degradation under normoxic conditions as a result of hydroxylation and subsequent polyubiquitination [295, 297, 302–305].”
BackgroundSTATs in cancer inflammation and immunity: a leading role for STAT3
Yu, H., Pardoll, D., & Jove, R. (2009) · Nature reviews. Cancer · doi:10.1038/nrc2734 · Cited by 4,383
Itoh, K., Chiba, T., Takahashi, S., Ishii, T., Igarashi, K., Katoh, Y., Oyake, T., Hayashi, N., Satoh, K., Hatayama, I., et al. (1997) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1997.6943 · Cited by 3,999
Itoh, K., Wakabayashi, N., Katoh, Y., Ishii, T., Igarashi, K., Engel, J. D., & Yamamoto, M. (1999) · Genes & Development · doi:10.1101/gad.13.1.76 · Cited by 3,634
Cited by
Conquering the Hypoxia Limitation for Photodynamic Therapy
Wan, Y., Fu, L., Li, C., Lin, J., & Huang, P. (2021) · Advanced Materials · doi:10.1002/adma.202103978 · Cited by 705
Overcoming barriers in photodynamic therapy harnessing nano-formulation strategies
Xie, J., Wang, Y., Choi, W., Jangili, P., Ge, Y., Xu, Y., Kang, J., Liu, L., Zhang, B., Xie, Z., et al. (2021) · Chemical Society Reviews · doi:10.1039/d0cs01370f · Cited by 522
Karimi, M., Sahandi Zangabad, P., Ghasemi, A., Amiri, M., Bahrami, M., Malekzad, H., Ghahramanzadeh Asl, H., Mahdieh, Z., Bozorgomid, M., Ghasemi, A., et al. (2016) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.6b00371 · Cited by 500
Self-citationLight Triggered Oxygen-Affording Engines for Repeated Hypoxia-Resistant Photodynamic Therapy
Zhou, T.-J., Xing, L., Fan, Y.-T., Cui, P.-F., & Jiang, H.-L. (2019) · Journal of Controlled Release · doi:10.1016/j.jconrel.2019.06.016 · Cited by 104
Weijer, R., Broekgaarden, M., Krekorian, M., Alles, L. K., van Wijk, A. C., Mackaaij, C., Verheij, J., van der Wal, A. C., van Gulik, T. M., Storm, G., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.6490 · Cited by 67
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Metadata
- Authors
- Broekgaarden, M., Weijer, R., van Gulik, T. M., Hamblin, M. R., & Heger, M.
- Venue
- Cancer and Metastasis Reviews
- Published
- 2015-10-29
- Volume
- 34
- Issue
- 4
- Pages
- 643-690
- ISSN
- 0167-7659 (ISSN-L)
- 1573-7233
- OpenAlex
- W1833716810
- Cited by
- 255
- References
- 58
- FWCI
- 3.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
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