ArticleJournal of molecular neuroscience : MN2015
Pygo2 siRNA Inhibit the Growth and Increase Apoptosis of U251 Cell by Suppressing Histone H3K4 Trimethylation.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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2 citing papers in PubMed, 5 citations in OpenAlex.
- Pygo2 as a novel biomarker in gastric cancer for monitoring drug resistance by upregulating MDR1.Journal of Cancer · 2021Article
- Pygopus2 inhibits the efficacy of paclitaxel-induced apoptosis and induces multidrug resistance in human glioma cells.Oncotarget · 2017Article
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9 authors at 3 institutions in 1 country.
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Abstract
The development of novel therapeutic strategies for glioma requires the identification of molecular targets involved in malignancy. Pygopus (Pygo) is a new discovered and specific downstream component of canonical Wnt signaling. Our previous study has demonstrated that Pygo2 is highly expressed in and promotes the growth of glioma cells. However, the role of Pygo2 in glioma remains to be elucidated. In the current study, we investigated the role of Pygo2 in human glioma U251 cells and showed that knocking down of the expression of Pygo2 in U251 cells using lentivirally expressed siRNA have inhibited cell proliferation and increased apoptosis through decreasing H3K4me3 expression. Moreover, we found Pygo2 was enriched in U251 glioma cancer stem-like cells and Pygo2 siRNA resulted in a reduced number as well as size of tumor spheres. According to our result, this paper now links mechanistically Pygo2's role in histone modification to its enhancement/reduction of proliferation/apoptosis in glioma cells and indicate that Pygo2 may play an important role in self-renew and proliferation in U251 glioma cancer stem-like cells.
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