GLIS family zinc finger 3 promoting cell malignant behaviors and NF-κB signaling in glioma

Liu, Zhuohang; Liu, Luochen; Qi, Yanan; Li, Hang; Pan, Shuyi

doi:10.1016/j.brainres.2021.147623

Cited by 11 publications

(9 citation statements)

References 27 publications

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“…15) Besides that, enhanced expression level of GLIS3 was shown in this work to reduce the levels of E-cadherin, while downregulation of GLIS3 inhibited the level of N-cadherin and vimentin. In Liu's study, 29) GLIS3 could promote the invasion, migration, and proliferation of glioma cell, which is same as ours. The accurate mechanisms of how GLIS3 improves migration and invasiveness have not been confirmed yet, but some studies indicated that it may be due to the stimulation of EMT.…”

Section: Discussionsupporting

confidence: 81%

“…Importantly, GLIS3 has been proved could promote cell malignant behaviors and NF-κB signaling pathway in glioma. 29) Based on these findings, we focused on NF-κB signaling pathway when exploring the potential mechanism of GLIS3 on TNBC progression. In Liu's research, 29) their results indicated that the abrogation of GLIS3 inhibited expression levels of p-p65, which subsequently affected the NF-κB signaling cascade, such as C-Myc and MMP9 in cells, and this trend could be partly counteracted by NF-κB overexpression.…”

Section: Discussionmentioning

confidence: 99%

“…29) Based on these findings, we focused on NF-κB signaling pathway when exploring the potential mechanism of GLIS3 on TNBC progression. In Liu's research, 29) their results indicated that the abrogation of GLIS3 inhibited expression levels of p-p65, which subsequently affected the NF-κB signaling cascade, such as C-Myc and MMP9 in cells, and this trend could be partly counteracted by NF-κB overexpression. Similar with their results, we found that GLIS3 enhanced the levels of p-p65 in TNBC cells and the addition of inhibitor (BAY11-7082) reversed this enhancement.…”

Section: Discussionmentioning

confidence: 99%

“…In previously reported studies, GLIS3 and its family member GLIS1-2 all have been reported were involved in the regulation of NF-κB signaling pathway in different cells and tissues. [29][30][31] Accordingly, IF staining assay was applied to investigate the effect of GLIS3 up/down-regulation in NF-κB p65 nuclear translocation. As we can see, in vector transfected cells, NF-κB p65 is mainly present in the cytoplasm, while obvious NF-κB p65 staining was shown in the nucleus of GLIS3-overexpressing cells (Fig.…”

Section: Glis3 Is Overexpressed In Tnbc Clinical Tissues Andmentioning

confidence: 99%

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GLIS Family Zinc Finger 3 Promotes Triple-Negative Breast Cancer Progression by Inducing Cell Proliferation, Migration and Invasion, and Activating the NF-κB Signaling Pathway

Geng

2023

Biological & Pharmaceutical Bulletin

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Triple-negative breast cancer (TNBC) puts a great threat to women's health. GLIS family zinc finger 3 (GLIS3) belongs to the GLI transcription factor family and acts as a critical factor in cancer progression. Nevertheless, the part of GLIS3 played in TNBC is not known. Immunohistochemical (IHC) staining analysis displayed that GLIS3 was highly expressed in TNBC tissues. The effect of GLIS3 on the malignant phenotype of TNBC was tested in two different cell lines according to GLIS3 regulation. Upregulation of GLIS3 promoted the proliferation, migration, and invasion of TNBC cell lines, whereas the knockdown of GLIS3 suppressed these tumor activities. Inhibition of GLIS3 induced TNBC cell apoptosis. Furthermore, study as immunofluorescence and electrophoretic mobility shift assay confirmed that the nuclear factor-κB (NF-κB) signaling pathway activated by GLIS3 played an important role in TNBC cells' malignant phenotype. In conclusion, the present work demonstrated that GLIS3 acts as a crucial element in TNBC progression via activating the NF-κB signaling pathway. Accordingly, above mentioned findings indicated that modulation of GLIS3 expression is a potential tactic to interfere with the progression of TNBC.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Glis3 Is Overexpressed In Tnbc Clinical Tissues Andmentioning

confidence: 99%

See 2 more Smart Citations

GLIS Family Zinc Finger 3 Promotes Triple-Negative Breast Cancer Progression by Inducing Cell Proliferation, Migration and Invasion, and Activating the NF-κB Signaling Pathway

Geng

2023

Biological & Pharmaceutical Bulletin

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“…Thus, circGLIS3 appears to promote the malignancy of gliomas by both increasing invasiveness and angiogenesis. A different report showed that high levels of GLIS3 expression correlated with high-grade gliomas and poor prognosis [ 116 ]. Knockdown of GLIS3 expression in glioma cells lines reduced cell proliferation and migration, inhibited the activation of the NF-κB signaling pathway, and suppressed the in vivo malignant behavior of cells when implanted into nude mice.…”

Section: Glis Circular Rnasmentioning

confidence: 99%

GLIS1-3: Links to Primary Cilium, Reprogramming, Stem Cell Renewal, and Disease

Jetten

Scoville

Kang

2022

Cells

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The GLI-Similar 1-3 (GLIS1-3) genes, in addition to encoding GLIS1-3 Krüppel-like zinc finger transcription factors, also generate circular GLIS (circGLIS) RNAs. GLIS1-3 regulate gene transcription by binding to GLIS binding sites in target genes, whereas circGLIS RNAs largely act as miRNA sponges. GLIS1-3 play a critical role in the regulation of many biological processes and have been implicated in various pathologies. GLIS protein activities appear to be regulated by primary cilium-dependent and -independent signaling pathways that via post-translational modifications may cause changes in the subcellular localization, proteolytic processing, and protein interactions. These modifications can affect the transcriptional activity of GLIS proteins and, consequently, the biological functions they regulate as well as their roles in disease. Recent studies have implicated GLIS1-3 proteins and circGLIS RNAs in the regulation of stemness, self-renewal, epithelial-mesenchymal transition (EMT), cell reprogramming, lineage determination, and differentiation. These biological processes are interconnected and play a critical role in embryonic development, tissue homeostasis, and cell plasticity. Dysregulation of these processes are part of many pathologies. This review provides an update on our current knowledge of the roles GLIS proteins and circGLIS RNAs in the control of these biological processes in relation to their regulation of normal physiological functions and disease.

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FAM83H regulated by glis3 promotes triple-negative breast cancer tumorigenesis and activates the NF-κB signaling pathway

Li,

Wang,

Shi

et al. 2024

J Mol Histol

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GLIS family zinc finger 3 promoting cell malignant behaviors and NF-κB signaling in glioma

Cited by 11 publications

References 27 publications

GLIS Family Zinc Finger 3 Promotes Triple-Negative Breast Cancer Progression by Inducing Cell Proliferation, Migration and Invasion, and Activating the NF-κB Signaling Pathway

GLIS Family Zinc Finger 3 Promotes Triple-Negative Breast Cancer Progression by Inducing Cell Proliferation, Migration and Invasion, and Activating the NF-κB Signaling Pathway

GLIS1-3: Links to Primary Cilium, Reprogramming, Stem Cell Renewal, and Disease

FAM83H regulated by glis3 promotes triple-negative breast cancer tumorigenesis and activates the NF-κB signaling pathway

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