Downregulation of SCAI enhances glioma cell invasion and stem cell like phenotype by activating Wnt/β-catenin signaling

Chen, Xiangrong; Hu, Weipeng; Xie, Baoyuan; Gao, Hongzhi; Xu, Chaoyang; Chen, Junyan

doi:10.1016/j.bbrc.2014.04.098

Cited by 34 publications

(25 citation statements)

References 20 publications

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“…SCAI 3'UTR was verified to be recognized by miR-766-5p. The present study demonstrated that SCAI was deregulated in tumor tissues compared with normal tissues, which was consistent with a previous study that also reported the decrease of SCAI in human cancer, implying a tumor suppressive role (20,21). In the present study, western blotting revealed that, following miR-766-5p inhibitor administration, SCAI protein level was upregulated in SW480 cells in comparison with the level in the NC group, demonstrating the interaction between miR-766-5p and SCAI.…”

Section: Discussionsupporting

confidence: 93%

The role of miR-766-5p in cell migration and invasion in colorectal cancer

2018

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Abstract. Colorectal cancer (CRC) develops from the colon or rectum and is the fourth highest inducer of cancer mortality. In the present study, cancer tissues and normal tissues were extracted from patients with CRC who were treated in the Affiliated Hospital of Shandong University of Traditional Chinese Medicine (Jinan, China). Reverse transcription-quantitative polymerase chain reaction demonstrated that the expression level of miR-766-5p was significantly higher (P<0.01) in cancer tissue than that in normal tissue. SW480 cells were used for in vitro study and randomly separated into the miR-negative control (NC) inhibitor treatment group and miR-766-5p inhibitor treatment group. SW480 cell behaviors were evaluated. Results demonstrated that in the miR-766-5p inhibitor group, there was a decreased level of cell proliferation/migration/invasion and higher cell apoptosis compared with that in the miR-NC inhibitor group. miR-766-5p was predicted and verified to target the 3' untranslated region of suppressor of cancer cell invasion (SCAI) in SW480 cells. Protein expression levels of matrix metalloproteinase-2/phosphoinositide 3-kinase/AKT were decreased and SCAI was increased following miR-766-5p inhibitor treatment. In conclusion, the present study indicated that miR-766-5p inhibitor repressed the process of CRC by targeting SCAI.

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Section: Discussionsupporting

confidence: 93%

The role of miR-766-5p in cell migration and invasion in colorectal cancer

2018

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“…Recently, Wnt/β-catenin was also found to contribute to the proliferation of glioblastoma cells and GSCs (Kim et al 2013;Zhang et al 2015). The research of Chen et al demonstrated that glioma cell aggressiveness and stem cell-like phenotype are correlated to activating Wnt/β-catenin pathway (Chen et al 2014b). Knockdown of Wnt/β-catenin signaling resulted in decreasing the invasions of GSCs (Gong and Huang 2012).…”

Section: Discussionmentioning

confidence: 96%

PI3K inhibitor combined with miR-125b inhibitor sensitize TMZ-induced anti-glioma stem cancer effects through inactivation of Wnt/β-catenin signaling pathway

Shi

Fei

Wang

et al. 2015

In Vitro Cell.Dev.Biol.-Animal

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Temozolomide (TMZ) is a promising chemotherapeutic agent for treating glioblastomas. However, resistance develops quickly with a high frequency. Glioblastoma stem cells (GSCs) causing resistance to drug therapy were considered to be one of the key factors. The mechanisms underlying GSCs resistance to TMZ are not fully understood. MicroRNAs (miRNAs) have emerged to play important roles in tumorigenesis and drug resistance. Our previous studies showed that miR-125b was necessary for GSCs fission, and inhibition of which could enhance the chemosensitivity of GSCs to TMZ. Recent studies have evidence that a variety of drugs and upstream factors work through PI3K/Akt pathway, and the effects of PI3K/Akt pathway inhibition on GSCs were much more than non-GSCs. In this study, we found that PI3K inhibitor combined with miR-125b inhibitor caused a marked increase of TMZ-induced GSC proliferation and invasiveness inhibition. To explore the potential mechanism, we found that this novel combinatorial regimen leads to changes of inactivation of Wnt/β-catenin pathway which regulates a series of cell activities including cell apoptosis, proliferation, differentiation, and metabolism. Taken together, our data strongly support an important role for PI3K inhibitor and miR-125b inhibitor on conferring GSCs resistance to TMZ through targeting Wnt/β-catenin signaling pathway.

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“…When fibroblasts differentiate into myofibroblast, the ability of synthesis ECM is enhanced and fibrosis proceeding is aggravated [36]. The importance of Wnt signaling in metastatic and invasive capacity is already demonstrated in many tumor cells [37,38]. Therefore, we used scarification essay and found that NSC668036 can remarkably depress the migration ability of fibroblasts.…”

Section: Discussionmentioning

confidence: 93%