SOX9 Overexpression Promotes Glioma Metastasis via Wnt/Œ≤-Catenin Signaling
Authors: Renjun Peng
Zhixiong Liu
Zhiming Ma
Hongwei Liu
Jingchen Lu
Bing Jiang
Journal: Cell Biochemistry and Biophysics (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cell migration; EMT; Invasion; Metastasis; SOX9
Affiliations: Department of Neurosurgery, Xiangya Hospital, Central South University (CSU), Changsha, China., Department of Oncology, Xiangya Hospital, Central South University (CSU), Changsha, China. .

Abstract:  SOX9 gene encodes a transcription factor essential for a central role in the development and differentiation of multiple cell lineages, such as in neurogenesis, neural crest development, etc. Recent study reported that overexpression of SOX9 mRNA is closely associated with poor clinical outcome of patients with malignant gliomas. In the present study, we have explored the regulatory role of SOX9 in glioma metastasis. To investigate the role of SOX9 in glioma metastasis, SOX9 overexpressed in human glioma cell line U251 on cell migration and invasion was evaluated via wound scratch, Transwell assay without or with Matrigel. SOX9-induced changes in EMT process were evaluated by Western blot. Furthermore, the role of Œ≤-catenin in the regulatory effect of SOX9 on cell migration and invasion, and EMT process was explored by suppressing Œ≤-catenin expression in SOX9-overexpressed U251 cells. SOX9 overexpression in U251 cells resulted in a significant increase in cell migration and invasion. SOX9 overexpression also markedly promoted the EMT process. More importantly, our results revealed that SOX9 stimulated metastasis through activating Wnt/Œ≤-catenin signaling. In summary, this study indicated that the promoting effect of SOX9 on glioma metastasis was, at least in part, through Wnt/Œ≤-catenin signaling. The findings in this study highlight the effectiveness and therapeutic potential to utilize SOX9 targeted strategies in the treatment of glioma. 

Retracted: No

PubPeer comments:
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 Correction to: Nature Cell Biology https: doi.org 10.1038 ncb3195, published online 6 July 2015 In the version of this Article originally published, several images in Fig. 6e and g were mislabeled. u201cGFP shRNAu201d should be added to all the panels in Fig. 6e, and u201cDMSOu201d should be added to all panels in Fig. 6g. The legend should also be updated accordingly as: u201ce, HCA2 cells were infected with a control lentivirus (LP3) or lentivirus carrying oncogenic RAS. Cells were cultured with vehicle (DMSO) for 10 days or drug (Rapa) for 3 days (acute) and switched to DMSO for an additional 7 days or continuously treated (chronic) for 10 days with Rapa. Thereafter, clonogenic assays were performed. f, HCA2 cells were co-infected with RAS and lentiviruses carrying shRNAs to deplete the indicated proteins. Transcript levels (relative to GFP shRNA) for IL6 were quantified by qPCR. g, The DMSO-treated cells described in e were additionally infected (co-infected) with shRNAs to deplete the indicated proteins; 10 days later, clonogenic assays were performed as described in e. h, HCA2 cells infected with lentiviruses carrying the indicated shRNAs were induced to senesce by ionizing radiation or were mock irradiated (NS, non-senescent). Clonogenic assays were performed 10 days later.u201d https: www.nature.com articles s41556-021-00655-4 , 
 #2 induction of senescence by ionising radiation is somewhat hard to digest. It doesn t match with the senescence process. Ionising radiation is a different type of genotoxic agent compared to chemicals. The damage can be persistent but it may not induce senescence. ,