ArticleInternational journal of molecular sciences2012
TRAIL and paclitaxel synergize to kill U87 cells and U87-derived stem-like cells in vitro.
Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Magnetic Fields in Cancer Therapy: Mechanistic Insights, Signaling Pathways, and Evidence from Clinical and In Vitro Studies.Pharmaceutics · 2026Review
- Tumor necrosis factor-related apoptosis-inducing ligand inhibits the growth and aggressiveness of colon carcinoma via the exogenous apoptosis signaling pathway.Experimental and therapeutic medicine · 2019Article
- Assessment of concentrations of sTRAIL ligand and its receptors sTRAIL-R1 and sTRAIL-R2 - markers monitoring the course of the extrinsic pathway of apoptosis induction: potential application in ovarian cancer diagnostics.Archives of medical science : AMS · 2017Article
- Wnt/β-catenin signaling pathway inhibits the proliferation and apoptosis of U87 glioma cells via different mechanisms.PloS one · 2017Article
- RNAi for contactin 2 inhibits proliferation of U87-glioma stem cells by downregulating AICD, EGFR, and HES1.OncoTargets and therapy · 2017Article
- The synergic antitumor effects of paclitaxel and temozolomide co-loaded in mPEG-PLGA nanoparticles on glioblastoma cells.Oncotarget · 2016Article
- Expression of a-disintegrin and metalloproteinase 10 correlates with grade of malignancy in human glioma.Oncology letters · 2015Article
- CYP1B1 enhances the resistance of epithelial ovarian cancer cells to paclitaxel in vivo and in vitro.International journal of molecular medicine · 2015Article
- Genetically engineered Newcastle disease virus expressing interleukin-2 and TNF-related apoptosis-inducing ligand for cancer therapy.Cancer biology & therapy · 2014Article
- N-(2-hydroxyphenyl)acetamide (NA-2) and Temozolomide synergistically induce apoptosis in human glioblastoma cell line U87.Cancer cell international · 2014Article
- Effect of all-trans retinoic acid on the differentiation of U87 glioma stem/progenitor cells.Cellular and molecular neurobiology · 2013Article
- Paclitaxel-Fe3O4 nanoparticles inhibit growth of CD138(-) CD34(-) tumor stem-like cells in multiple myeloma-bearing mice.International journal of nanomedicine · 2013Article
- Targeting death receptor TRAIL-R2 by chalcones for TRAIL-induced apoptosis in cancer cells.International journal of molecular sciences · 2012Article
- Current approaches in enhancing TRAIL therapies in glioblastoma.Neuro-oncology advancesReview
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
U87-derived stem-like cells (U87-SLCs) were cultured using serum-free stem cell media and identified by both biological behaviors and markers. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and paclitaxel (PX), in combination or alone, was used to treat U87-MG human glioma cells (U87 cells) or U87-SLCs. The results showed that TRAIL/PX cannot only synergistically inhibit U87 cells but also U87-SLCs. We observed a significantly higher apoptotic rate in U87 cells simultaneously treated with TRAIL/PX for 24 h compared to cells treated with either drug alone. Furthermore, there was a remarkably higher apoptosis rate in U87-SLCs induced by the TRAIL/PX combination compared with either drug alone. Unlike the simultaneous treatment in U87 cells, U87-SLCs were pretreated for 24 h with 1 μmol/L of PX followed by 1000 ng/mL of TRAIL. Protein assays revealed that TRAIL/PX synergy was related to DR4, cleaved caspase-8 and cleaved caspase-3 upregulation, whereas the mitochondrial pathway was not involved in TRAIL-induced apoptosis. The present study indicates that PX can sensitize U87 cells and U87-SLCs to TRAIL treatment through an extrinsic pathway of cell apoptosis. The combined treatment of TRAIL and PX may be a promising glioma chemotherapy because of its successful inhibition of U87-SLCs, which are hypothesized to influence chemotherapeutic outcomes of gliomas.
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