Overexpression of SCUBE2 Inhibits Proliferation, Migration, and Invasion in Glioma Cells

Guo, Erkun; Liu, Hongjiang; Liu, Xiaopeng

doi:10.3727/096504016x14747335734344

Cited by 14 publications

(8 citation statements)

References 30 publications

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“…The signal peptide CUB EGF-like domain-containing protein 2 (SCUBE2), a member of the SCUBE family of proteins, inhibits cell proliferation and migration in glioma stem cells by downregulating Hh signaling. 265 BCL6, a transcriptional repressor and lymphoma oncoprotein, directly represses the Sonic Hh effectors Gli1 and Gli2 in medulloblastoma stem cells. 266 The transcription factor RUNX3 suppresses metastasis and the stemness of colorectal CSCs by promoting ubiquitination of Gli1 at the intracellular level.…”

Section: Major Signaling Pathways In Cscsmentioning

confidence: 99%

Targeting cancer stem cell pathways for cancer therapy

Yang

Shi

Zhao

et al. 2020

Sig Transduct Target Ther

1,211

998

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Since cancer stem cells (CSCs) were first identified in leukemia in 1994, they have been considered promising therapeutic targets for cancer therapy. These cells have self-renewal capacity and differentiation potential and contribute to multiple tumor malignancies, such as recurrence, metastasis, heterogeneity, multidrug resistance, and radiation resistance. The biological activities of CSCs are regulated by several pluripotent transcription factors, such as OCT4, Sox2, Nanog, KLF4, and MYC. In addition, many intracellular signaling pathways, such as Wnt, NF-κB (nuclear factor-κB), Notch, Hedgehog, JAK-STAT (Janus kinase/signal transducers and activators of transcription), PI3K/AKT/mTOR (phosphoinositide 3-kinase/AKT/mammalian target of rapamycin), TGF (transforming growth factor)/SMAD, and PPAR (peroxisome proliferator-activated receptor), as well as extracellular factors, such as vascular niches, hypoxia, tumor-associated macrophages, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, extracellular matrix, and exosomes, have been shown to be very important regulators of CSCs. Molecules, vaccines, antibodies, and CAR-T (chimeric antigen receptor T cell) cells have been developed to specifically target CSCs, and some of these factors are already undergoing clinical trials. This review summarizes the characterization and identification of CSCs, depicts major factors and pathways that regulate CSC development, and discusses potential targeted therapy for CSCs.Signal Transduction and Targeted Therapy (2020) 5:8; https://doi.

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Section: Major Signaling Pathways In Cscsmentioning

confidence: 99%

Targeting cancer stem cell pathways for cancer therapy

Yang

Shi

Zhao

et al. 2020

Sig Transduct Target Ther

1,211

998

View full text Add to dashboard Cite

show abstract

“…Despite improvements in surgical resection techniques combined with radiotherapy and chemotherapy, the prognosis of patients with advanced glioma remains poor ( 3 , 4 ). Deregulation of oncogenes or tumor suppressors has been implicated in the development and malignant progression of glioma, and some have been suggested as potential targets for glioma treatment ( 5 – 7 ).…”

Section: Introductionmentioning

confidence: 99%

Methylation-induced downregulation and tumor-suppressive role of microRNA-98 in glioma through targeting Sal-like protein 4

et al. 2018

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MicroRNAs (miRs) have been found to play key roles in various human cancers, but the detailed regulatory mechanism of miR-98 in glioma remains largely unknown. The findings of the present study demonstrated that miR-98 was frequently downregulated in glioma tissues and cell lines (U87, U251, U373 and SHG44), and the decreased miR-98 levels were associated with DNA methylation. Treatment with 5-Aza-20-deoxycytidine, a DNA methyltransferase inhibitor, significantly increased the expression of miR-98 in glioma cells. Moreover, both miR-98 downregulation and methylation were significantly associated with a more aggressive tumor phenotype in glioma, as well as shorter survival time of glioma patients. Restoration of miR-98 expression caused a marked decrease in the migration and invasion of U87 cells, but did not affect cell proliferation. Sal-like protein 4 (SALL4) was further identified as a novel target gene of miR-98, and its protein expression was negatively regulated by miR-98 in U87 cells. Restoration of SALL4 expression reversed the suppressive effects of miR-98 on the migration and invasion of U87 cells. Furthermore, SALL4 was significantly upregulated in glioma tissues and cell lines, and an inverse correlation between miR-98 and SALL4 expression in glioma tissues was identified. In addition, the increased expression of SALL4 was significantly associated with glioma progression. Taken together, these data demonstrated that downregulation of miR-98, induced by methylation, promotes glioma cell migration and invasion via targeting SALL4. Therefore, miR-98 may become a potential therapeutic candidate for glioma.

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“…(Cheng et al 2009)SCUBE2 also performed as protective factor in glioma, non-small cell lung cancer and colorectal cancer and inhibited the proliferation and migration. (Guo et al 2017;Song et al 2015;Yang et al 2018) The Wnt secretion protein Wntless (WLS) has been proved to be involved in the development of several human cancers. WLS mostly plays the role of oncogene in most tumors.…”

Section: Discussionmentioning

confidence: 99%

Peer Review #1 of "Estrogen receptor—positive breast cancer survival prediction and analysis of resistance–related genes introduction (v0.1)"

2021

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Overexpression of SCUBE2 Inhibits Proliferation, Migration, and Invasion in Glioma Cells

Cited by 14 publications

References 30 publications

Targeting cancer stem cell pathways for cancer therapy

Targeting cancer stem cell pathways for cancer therapy

Methylation-induced downregulation and tumor-suppressive role of microRNA-98 in glioma through targeting Sal-like protein 4

Peer Review #1 of "Estrogen receptor—positive breast cancer survival prediction and analysis of resistance–related genes introduction (v0.1)"

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