ArticleMolecular and cellular biochemistry2012
9-phenyl acridine exhibits antitumour activity by inducing apoptosis in A375 cells.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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Who cites it
6 citing papers in PubMed, 28 citations in OpenAlex.
- Acridine-derived small molecule associates with VEGF and is linked to reduced CAM vascularization: a combined in silico and CAM study.BMC pharmacology & toxicology · 2026Article
- Acridine as an Anti-Tumour Agent: A Critical Review.Molecules (Basel, Switzerland) · 2022Review
- Ameliorative effects of 9-diaminoacridine derivative against Ehrlich ascites carcinoma-induced hepatorenal injury in mice.Environmental science and pollution research international · 2021Article
- Article
- INHIBITION OF PACLITAXEL AGAINST NEUROGLIOMA CELLS U251 GROWTH AND ITS MECHANISM.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2017Article
- Acridine yellow G blocks glioblastoma growth via dual inhibition of epidermal growth factor receptor and protein kinase C kinases.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several acridine derivatives have been screened for their therapeutic potential and some are already established as antiprotozoan, antibacterial or anticancer agents. However, phenyl derivative at C-9 position of acridine had remained unexplored for their biological activity so far. In this report, we present our findings with 9-phenyl acridine (ACPH) as an anticancer agent. Both A375 and HeLa, two human cancer cell lines, were more sensitive to ACPH than normal cells namely human lymphocytes and also Chinese hamster V79 cells. ACPH also led to regression of tumour volume in mice. In A375 cells, we have shown that it caused DNA damage and blocked cell cycle progression at G(2)-M phase. Treatment with ACPH led to lowering of mitochondrial potential, upregulation of bax, release of cytochrome C and activation of caspase 3. As a new agent showing lower toxicity to normal cells and greater sensitivity towards cancerous cell line, ACPH shows promise as an effective cancer chemotherapeutic agent. ACPH treatment resulted in apoptotic death of cells through mitochondria-mediated caspase-dependent pathway.
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Registered trials
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