Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/ijms22115697
Keywords
lung carcinogenesis; phytochemicals; cancer stem cell; epigallocatechin-3-gallate; sulforaphane
Funding
- UCSI Research Excellence and Innovation Grant [REIG-FMS2020/009]
- Ministry of Higher Education, Malaysia [FRGS/1/2020/SKK0/UCSI/02/2]
- Graduate School of Medical Sciences, University Medical Center Groningen, The Netherlands
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Lung cancer, one of the deadliest cancers, can be effectively reduced through prevention measures, though treatment improvements are still needed to address therapeutic resistance caused by cancer stem cells; phytochemicals in plant-based diets are believed to have efficacy in targeting lung cancer stem cells.
Lung cancer is still one of the deadliest cancers, with over two million incidences annually. Prevention is regarded as the most efficient way to reduce both the incidence and death figures. Nevertheless, treatment should still be improved, particularly in addressing therapeutic resistance due to cancer stem cells-the assumed drivers of tumor initiation and progression. Phytochemicals in plant-based diets are thought to contribute substantially to lung cancer prevention and may be efficacious for targeting lung cancer stem cells. In this review, we collect recent literature on lung homeostasis, carcinogenesis, and phytochemicals studied in lung cancers. We provide a comprehensive overview of how normal lung tissue operates and relate it with lung carcinogenesis to redefine better targets for lung cancer stem cells. Nine well-studied phytochemical compounds, namely curcumin, resveratrol, quercetin, epigallocatechin-3-gallate, luteolin, sulforaphane, berberine, genistein, and capsaicin, are discussed in terms of their chemopreventive and anticancer mechanisms in lung cancer and potential use in the clinic. How the use of phytochemicals can be improved by structural manipulations, targeted delivery, concentration adjustments, and combinatorial treatments is also highlighted. We propose that lung carcinomas should be treated differently based on their respective cellular origins. Targeting quiescence-inducing, inflammation-dampening, or reactive oxygen species-balancing pathways appears particularly interesting.
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