2016
DOI: 10.1016/j.jdermsci.2015.12.011
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Imiquimod activates p53-dependent apoptosis in a human basal cell carcinoma cell line

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Cited by 47 publications
(43 citation statements)
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“…El-Khattouti et al hypothesized that ER stress pathways are mediated through TLR7 activation [21], however we could not detect any expression of TLR7 in our cell lines prior to or after imiquimod treatment. As previous studies have also reported TLR7 independent activation of apoptosis in imiquimod treated tumour cell lines [13, 15, 18, 19, 37], we suggest imiquimod induces ER stress via alternative mechanisms.…”
Section: Discussionsupporting
confidence: 72%
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“…El-Khattouti et al hypothesized that ER stress pathways are mediated through TLR7 activation [21], however we could not detect any expression of TLR7 in our cell lines prior to or after imiquimod treatment. As previous studies have also reported TLR7 independent activation of apoptosis in imiquimod treated tumour cell lines [13, 15, 18, 19, 37], we suggest imiquimod induces ER stress via alternative mechanisms.…”
Section: Discussionsupporting
confidence: 72%
“…These findings reflect the high amounts of imiquimod required for the immunotherapy of superficial basal carcinoma in humans, with FDA guidelines suggesting topical application of 0.5–2 mg of imiquimod almost daily [42]. It has been suggested that apoptotic pathways in imiquimod treated tumour cells are activated as a result of ROS accumulation, which enhances ASK-1 stimulation of JNK and p38 apoptotic pathways [18, 21, 37, 4345]. Imiquimod-induced ROS production may occur as a result of calcium induced deregulation of oxidative phosphorylation [21], and rapid accumulation is likely due to the elevated metabolic activity of tumour cells.…”
Section: Discussionmentioning
confidence: 73%
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“…Further study revealed that expression of Bcl-2 was downregulated and cleavage of caspase-3, caspase-7 was upregulated in imiquimod-treated cells (Smits et al, 2010), suggesting that the apoptosis-inducing effects of imiquimod were involved in a caspase-dependent mitochondrial pathway. Futhermore, imiquimod induced reactive oxygen species production to stimulate ATM/ATR pathways and lead to p53-dependent apoptosis in the skin basal cell carcinoma cells (Huang et al, 2016). However, there were no available studies testifying that MYD88 pathway activates p53 expression.…”
Section: Anti-tumor Mechanismmentioning
confidence: 99%
“…ADORA promotes PKA activity leading to the phosphorylation of GLI and the selection of the repressor form of GLI . Imiquimod has been shown to stimulate p53‐induced apoptosis through increased ROS production and stimulation of the ATM/ATR . However, this mechanism may not operate in BCCs carrying mutant p53.…”
Section: Interventionsmentioning
confidence: 99%