scholarly journals Correction: Pigment Epithelium-Derived Factor (PEDF) Expression Induced by EGFRvIII Promotes Self-renewal and Tumor Progression of Glioma Stem Cells

PLoS Biology ◽  
2016 ◽  
Vol 14 (1) ◽  
pp. e1002367 ◽  
Author(s):  
Jinlong Yin ◽  
Gunwoo Park ◽  
Tae Hoon Kim ◽  
Jun Hee Hong ◽  
Youn-Jae Kim ◽  
...  
PLoS Biology ◽  
2015 ◽  
Vol 13 (5) ◽  
pp. e1002152 ◽  
Author(s):  
Jinlong Yin ◽  
Gunwoo Park ◽  
Tae Hoon Kim ◽  
Jun Hee Hong ◽  
Youn-Jae Kim ◽  
...  

2015 ◽  
Vol 16 (3) ◽  
pp. 219-220 ◽  
Author(s):  
Yu Shi ◽  
Yi-fang Ping ◽  
Xia Zhang ◽  
Xiu-wu Bian

2020 ◽  
Vol 34 (4) ◽  
pp. 5128-5143
Author(s):  
Lilei Peng ◽  
Yang Ming ◽  
Ling Zhang ◽  
Jie Zhou ◽  
Wei Xiang ◽  
...  

2021 ◽  
Author(s):  
Zhi Huang ◽  
Kui Zhai ◽  
Qiulian Wu ◽  
Xiaoguang Fang ◽  
Qian Huang ◽  
...  

Glioblastoma (GBM) is the most lethal brain tumor containing glioma stem cells (GSCs) that promote malignant growth and therapeutic resistance. The self-renewal and tumorigenic potential of GSCs are maintained by core stem cell transcription factors including SOX2. Defining the posttranslational regulation of SOX2 may offer new insights into GSC biology and potential therapeutic opportunity. Here, we discover that HAUSP stabilizes SOX2 through deubiquitination to maintain GSC self-renewal and tumorigenic potential. HAUSP is preferentially expressed in GSCs in perivascular niches in GBMs. Disrupting HAUSP by shRNA or its inhibitor P22077 promoted SOX2 degradation, induced GSC differentiation, impaired GSC tumorigenic potential, and suppressed GBM tumor growth. Importantly, pharmacological inhibition of HAUSP synergized with radiation to inhibit GBM growth and extended animal survival, indicating that targeting HAUSP may overcome GSC-mediated radioresistance. Our findings reveal an unappreciated crucial role of HAUSP in the GSC maintenance and provide a promising target for developing effective anti-GSC therapeutics to improve GBM treatment.


2015 ◽  
Vol 3 (S2) ◽  
Author(s):  
Prahlad Parajuli ◽  
Rohit Anand ◽  
Chandramouli Mandalaparty ◽  
Raviteja Suryadevara ◽  
Preethi Sriranga ◽  
...  

BMC Cancer ◽  
2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Jianhong Zhu ◽  
Handong Wang ◽  
Qing Sun ◽  
Xiangjun Ji ◽  
Lin Zhu ◽  
...  

2015 ◽  
Vol 362 (3) ◽  
pp. 611-621 ◽  
Author(s):  
Hongliang Liang ◽  
Weixun Duan ◽  
Huiyuan Hou ◽  
Wei Yi ◽  
Jinzhou Zhang ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Xin Chen ◽  
Qiyun Yang ◽  
Tao Zheng ◽  
Jun Bian ◽  
Xiangzhou Sun ◽  
...  

The paracrine effect is the major mechanism of stem cell therapy. However, the details of the effect’s mechanism remain unknown. The aim of this study is to investigate whether adipose tissue-derived stem cells (ADSCs) can ameliorate cavernous nerve injury-induced erectile dysfunction (CNIED) rats and to determine its mechanism. Twenty-eight days after intracavernous injection of 5-ethynyl-2-deoxyuridine- (EdU-) labeled ADSCs, the erectile function of all the rats was evaluated by intracavernosal pressure (ICP). The ADSCs steadily secreted detectable pigment epithelium-derived factor (PEDF)in vitro. The expression of PEDF increased in the penis of the bilateral cavernous nerve injury (BCNI) group for 14 days and then gradually decreased. On day 28 after the intracavernous injection, the ADSCs group exhibited a significantly increased ICP compared with the phosphate buffered saline- (PBS-) treated group. Moreover, the neuronal nitric oxide synthase (nNOS) and S100 expression in penile dorsal nerves and the smooth muscle content to collagen ratio in penile tissues significantly increased. Furthermore, elevated PEDF, p-Akt, and p-eNOS were identified in the ADSCs group. This study demonstrated that intracavernous injection of ADSCs improved erectile function, repaired the nerve, and corrected penile fibrosis. One potential mechanism is the PEDF secretion of ADSCs and subsequent PI3K/Akt pathway activation.


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