ArticleInternational journal of oncology2010
Cucurbitacin B inhibits growth, arrests the cell cycle, and potentiates antiproliferative efficacy of cisplatin in cutaneous squamous cell carcinoma cell lines.
Article in International journal of oncology, 2010. 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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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, 31 citations in OpenAlex.
- Bitter Phytochemicals as Novel Candidates for Skin Disease Treatment.Current issues in molecular biology · 2023Review
- Cucurbitacin B and cisplatin induce the cell death pathways in MB49 mouse bladder cancer model.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Synthesis of Cucurbitacin B Derivatives as Potential Anti-Hepatocellular Carcinoma Agents.Molecules (Basel, Switzerland) · 2018Article
- Approach for chemosensitization of cisplatin-resistant ovarian cancer by cucurbitacin B.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Cucurbitacin B induced ATM-mediated DNA damage causes G2/M cell cycle arrest in a ROS-dependent manner.PloS one · 2014Article
- The triterpenoid cucurbitacin B augments the antiproliferative activity of chemotherapy in human breast cancer.International journal of cancer · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cutaneous squamous cell carcinoma (CSCC) is the second most common skin cancer with a substantial risk of metastasis which causes clinical treatment failure. This study investigated the anti-CSCC effects of a triterpenoid compound, Cucurbitacin B (CuB). Dose-response studies showed that CuB inhibited 50% growth (ED50) of the CSCC cell lines (SRB1, SRB12, SCC13, COLO16) in liquid culture at 4 x 10(-7)-10(-5) M. Soft-agar assays demonstrated that nearly all of the CSCC clonogenic cells were inhibited at 10(-7) M CuB. FACS analysis found that the compound (10(-7) M, 48 h) caused G2/M arrest. The CSCC cells underwent profound morphologic changes within 60 min after exposure to CuB (10(-7) M), rounding up and losing their pseudopodia. CuB (10(-7) M) caused prominent multinucleation of the cells after they were pulse-exposed (24 h) to the drug, washed and cultured in normal medium for an additional 24 h. The drug (10(-8)-10(-6) M, 3-24 h) decreased levels of CDC2 and cyclin B1 in SRB1 and SRB12 cell lines as seen by Western blot analysis. Migration of SRB1 and SRB12 cells was inhibited by 10(-7) M CuB. Interestingly, CuB synergistically potentiated the anti-proliferative effect of cisplatin in CSCC. In summary, CuB has a prominent anti-proliferative activity on CSCC cells. In vivo studies and clinical trials of this drug should be pursued in CSCC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.