Stimulatory effect of oral administration of tea, coffee or caffeine on UVB-induced apoptosis in the epidermis of SKH-1 mice

Conney, Allan H.; Zhou, Sherry; Lee, Mao-Jung; Xie, Junshan; Yang, Chung S.; Lou, You-Rong; Lu, Yao-Ping

doi:10.1016/j.taap.2006.11.001

Cited by 48 publications

(33 citation statements)

References 13 publications

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“…The ATR-mediated DNA damage response not only activates cell cycle checkpoints but also regulates replication and different tolerance pathways, and ATR is a vital kinase for protecting the genome against DNA damage that blocks replication. Inhibiting ATR has the potential to protect against UVB-induced carcinogenesis (Conney et al, 2007) and is growing as a potential sensitizer of chemotherapy or radiation, with selective killing of p53-deficient cancer cells (Reaper et al, 2011;Peasland et al, 2011;Prevo et al, 2012;Sultana et al, 2013). Thus, knowledge of the ATR-mediated DNA damage response can also aid in the design of more efficient cancer treatment protocols.…”

Section: Discussionmentioning

confidence: 99%

ATR suppresses apoptosis after UVB light by controlling both translesion synthesis and alternative tolerance pathways

Andrade-Lima

Andrade

Menck

2014

Journal of Cell Science

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Ultraviolet (UV) light can stall replication forks owing to the formation of bulky lesions in the DNA. Replication across these blocking lesions occurs through translesion DNA synthesis, and cells activate the ATR damage responses to UV. However, it remains unclear whether lesion bypass requires the replication checkpoint because ATR is not necessary for PCNA ubiquitylation. We observed that ATR knockdown by siRNA increased replication stress and promoted early induction of apoptosis following UVB irradiation in SV40-immortalized human cells, including cells from XP-V and XP-C patients. XP-V cells were further sensitized by the silencing, indicating that DNA polymerase g (Pol g) remains active despite ATR control. However, following UVB irradiation, ATR-depleted cells were unable to achieve mitosis, as would be expected after the loss of a DNA checkpoint control. Thus, ATR also regulates replication arrest recovery following UVB-induced damage, independently of Pol g, in SV40-immortalized cell lines. The ATR-mediated DNA damage response regulates replication and different tolerance pathways, and in these cells, ATR depletion induces replication catastrophe, which contributes to explain the potential of ATR inhibition to protect against UVB-induced carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

ATR suppresses apoptosis after UVB light by controlling both translesion synthesis and alternative tolerance pathways

Andrade-Lima

Andrade

Menck

2014

Journal of Cell Science

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“…If the DNA damage is not repaired or the damaged cells are not eliminated by apoptosis, the consequences can be cell transformation, uncontrolled proliferation, and eventually skin Family history of melanoma, % 3 tumor formation (29). Mouse studies have shown that oral or topical caffeine administration promotes elimination of UVdamaged keratinocytes (the cells from which nonmelanoma skin cancer arises) via apoptosis and markedly reduces the risk of subsequent skin cancer development (8,(30)(31)(32). The mechanisms and molecular targets for the proapoptotic effect of caffeine after DNA damage have been investigated in cultured cell lines (human osteosarcoma cells).…”

Section: Discussionmentioning

confidence: 99%

Increased Caffeine Intake Is Associated with Reduced Risk of Basal Cell Carcinoma of the Skin

Song

Qureshi²,

Han³

2012

Cancer Research

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Studies in animals suggest that caffeine administration helps prevent squamous cell skin cancer development, but there have been limited epidemiologic studies on the association between caffeine consumption and skin cancer risk. Using data from the Nurses' Health Study and the Health Professionals Follow-up Study, we prospectively examined risks of basal cell carcinoma (BCC, 22,786 cases), squamous cell carcinoma (SCC, 1,953 cases), and melanoma (741 cases) in relation to caffeine intake. Cox proportional hazard models were used to calculate relative risks (RR) and 95% confidence intervals (CI). The amount of caffeine intake from all dietary sources was inversely associated with BCC risk. Compared with the lowest quintile, the highest quintile had the lowest risk (RR, 0.82 in women; 95% CI:,0.77-0.86 and RR, 0.87 in men; 95% CI, 0.81-0.94; P trend < 0.0001 in both). A significant inverse association was also found between caffeinated coffee consumption and BCC risk. Compared with individuals who consumed caffeinated coffee less than 1 cup per month, women who consumed more than 3 cups/d had the lowest risk (RR, 0.79; 95% CI, 0.74-0.85; P trend < 0.0001) and the RR for men was 0.90 (95% CI, 0.80-1.01; P trend ¼ 0.003). Caffeine from other dietary sources (tea, cola, and chocolate) was also inversely associated with BCC risk. Decaffeinated coffee consumption was not associated with a similar decrease in BCC risk. In contrast, caffeine intake was not found to be inversely associated with risks of SCC or melanoma. Our findings argue that caffeine intake in men and women is inversely associated with risk of BCC. Cancer Res; 72(13); 3282-9. Ó2012 AACR.

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“…It inhibits phosphodiesterase activity, alters intracellular calcium levels, inhibits phosphatidylinositol-3-kinase (PI3K) activity, antagonizes adenosine receptors, increases levels of cAMP, and activates cAMP-dependent protein kinase (PKA) (Daly and Fredholm, 1998;Fredholm et al, 1999;Gabrielli et al, 2007). Recently, many studies reported that caffeine has anti-cancer effects through the induction of apoptosis and suppression of cell proliferation (Bode and Dong, 2007) in several cancer types, including neuroblastoma (Jang et al, 2002), lung adenocarcinoma (Okano et al, 2008), and skin cancer (Conney et al, 2007;Hashimoto et al, 2004). Caffeine has also been reported to induce p53-independent G 1 -phase arrest in lung adenocarcinoma cell lines (Qi et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Caffeine Inhibits Cell Proliferation and Regulates PKA/GSK3β Pathways in U87MG Human Glioma Cells

Lee

Jeong

et al. 2011

Molecules and Cells

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Stimulatory effect of oral administration of tea, coffee or caffeine on UVB-induced apoptosis in the epidermis of SKH-1 mice

Cited by 48 publications

References 13 publications

ATR suppresses apoptosis after UVB light by controlling both translesion synthesis and alternative tolerance pathways

ATR suppresses apoptosis after UVB light by controlling both translesion synthesis and alternative tolerance pathways

Increased Caffeine Intake Is Associated with Reduced Risk of Basal Cell Carcinoma of the Skin

Caffeine Inhibits Cell Proliferation and Regulates PKA/GSK3β Pathways in U87MG Human Glioma Cells

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