ArticleOncogene2014
CTSL2 is a pro-apoptotic target of E2F1 and a modulator of histone deacetylase inhibitor and DNA damage-induced apoptosis.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Causal relationship between cathepsins and major salivary gland neoplasms: a bidirectional Mendelian randomization study.Gland surgery · 2024Article
- New inhibitors of cathepsin V impair tumor cell proliferation and elastin degradation and increase immune cell cytotoxicity.Computational and structural biotechnology journal · 2022Article
- Article
- Elevated CTSL2 expression is associated with an adverse prognosis in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2018Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant regulation of the pRB/E2F1 pathway has been invariably linked to inappropriate proliferation and/apoptosis in human cancers. Therefore, understanding the intricacies of the signaling pathway and identification of novel E2F1 targets involved in apoptosis could pave way for new therapeutic manipulation. Here, we identified CTSL2 (cathepsin L2/cathepsin V) as a novel E2F1 target that participates in E2F1-dependent apoptosis. We showed that E2F1 directly binds to CTSL2 promoter and that CTSL2 is regulated by both exogenous and endogenous E2F1. RNAi-mediated depletion of CTSL2 effectively abrogated ectopic E2F1-induced apoptosis, coupled with reduced lysosomal membrane permeabilization (LMP) and mitochondrial membrane depolarization. CTSL2 knockdown also inhibited apoptosis mediated by the endogenous E2F1 activated by DNA damage. Furthermore, we showed that CTSL2 depletion in cancer cells resulted in inhibition of histone deacetylase inhibitor (HDACi)-induced apoptosis, and conversely ectopic overexpression of CTSL2-sensitized cancer cells to HDACi. This study uncovered a novel E2F1 target implicated in LMP and apoptosis activation, as well as in the modulation of HDACi and chemotherapeutic drugs response.
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Registered trials
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