ArticleScientific reports2014
GADD45γ induces G2/M arrest in human pharynx and nasopharyngeal carcinoma cells by cucurbitacin E.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Sulforaphane-Induced Cell Mitotic Delay and Inhibited Cell Proliferation via Regulating CDK5R1 Upregulation in Breast Cancer Cell Lines.Biomedicines · 2023Article
- Perspectives on natural compounds in chemoprevention and treatment of cancer: an update with new promising compounds.European journal of cancer (Oxford, England : 1990) · 2021Review
- Identification and characterization of the Cucurbitacins, a novel class of small-molecule inhibitors of Tropomyosin receptor kinase a.BMC complementary and alternative medicine · 2019Article
- The effects of cucurbitacin E on GADD45β-trigger G2/M arrest and JNK-independent pathway in brain cancer cells.Journal of cellular and molecular medicine · 2019Article
- Inducement of apoptosis by cucurbitacin E, a tetracyclic triterpenes, through death receptor 5 in human cervical cancer cell lines.Cell death discovery · 2017Article
- Induction of Apoptosis in Endometrial Cancer (Ishikawa) Cells by Pogostemon cablin Aqueous Extract (PCAE).International journal of molecular sciences · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Nasopharyngeal carcinoma (NPC) is a common form of malignant cancer, for which radiotherapy or chemotherapy are the main treatment methods. Cucurbitacin E (CuE) is a natural compound-based drug which from the climbing stem of Cucumic melo L (Guadi). Previously shown to be an antifeedant as well as a potent chemopreventive agent against several types of cancer. The present study, investigated anti-proliferation and cell cycle G2/M arrest induced by CuE in Detroit 562 cells (pharynx carcinoma) and HONE-1 (nasopharyngeal carcinoma) cells. Results indicate that the cytotoxicity is associated with accumulation in G2/M cell-cycle phases. CuE produced cell cycle arrest as well as the downregulation of cyclin B1 and CDC2 expression. In addition, treated cells with CuE and GADD45γ SiRNA that also coincided with GADD45γ gene activation in cell cycle arrest. Both effects increased proportionally with the dose of CuE; however, proliferation inhibition and mitosis delay was dependant on the amount of CuE treatment in the cancer cells.
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