GATA4 promotes hepatoblastoma cell proliferation by altering expression of miR125b and DKK3

Pei, Yihua; Yao, Qing; Yuan, Sibo; Xie, Bozhen; Liu, Yan; Yang, Chunsheng; Zhuo, Huiqin

doi:10.18632/oncotarget.12839

Cited by 16 publications

(23 citation statements)

References 42 publications

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“…Moreover, Fang et al showed that silencing of GATA-6 resulted in decreased the expression of important mediators including MMP-2 and MMP-9 [31]. Also, a previous study has shown that GATA4 promoted oncogenesis through suppression of DKK3 expression in hepatoma cells [32]. MMP-2 and MMP-9 are enzymes involved in prostatic development and growth, important to cancer progression [33].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

Wei

2020

Cancer Cell Int

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Background Prostate cancer is one of the leading causes of cancer death in males. Recent studies have reported aberrant expression of lncRNAs in prostate cancer. This study explores the role of LINC00261 in prostate cancer progression. Methods The differentially expressed genes, transcription factors, and lncRNAs related to prostate cancer were predicted by bioinformatics analysis. Prostate cancer tissue samples and cell lines were collected for the determination of the expression of LINC00261 by reverse transcription quantitative polymerase chain reaction. The binding capacity of LINC00261 to the transcription factor GATA6 was detected by RIP, and GATA6 binding to the DKK3 promoter region was assessed by ChIP. In addition, luciferase reporter system was used to verify whether LINC00261 was present at the DKK3 promoter. After gain- and loss-of function approaches, the effect of LINC00261 on prostate cancer in vitro and in vivo was assessed by the determination of cell proliferation, invasion and migration as well as angiogenesis. Results LINC00261, GATA6, and DKK3 were poorly expressed in prostate cancer. LINC00261 could inhibit transcriptional expression of DKK3 by recruiting GATA6. Overexpression of LINC00261 inhibited prostate cancer cells proliferation, migration, and invasion as well as angiogenesis, which could be reversed by silencing DKK3. Furthermore, LINC00261 could also suppress the tumorigenicity of cancer cells in vivo. Conclusions Our study demonstrates the inhibitory role of LINC00261 in prostate cancer progression, providing a novel biomarker for early detection of prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

Wei

2020

Cancer Cell Int

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“…A recent report suggested that GATA4 may facilitate hepatoblastoma cell proliferation by regulating the expression of DKK3 and microRNA (miRNA) miR125b (40). A number of other studies have also demonstrated that miRNAs and transcription factors are closely correlated in gene regulatory networks (41), and bioinformatics analyses suggested that the promoter sequences of most mammalian miRNA genes included at least one GATA box, which indicated that GATA4 may transcriptionally regulate certain miRNAs.…”

Section: Discussionmentioning

confidence: 99%

GATA4 is highly expressed in childhood acute lymphoblastic leukemia, promotes cell proliferation and inhibits apoptosis by activating BCL2 and MDM2

Han

et al. 2017

Molecular Medicine Reports

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Members of the GATA‑binding factor protein family, including GATA1, GATA2 and GATA3, serve an inhibiting role in leukemia. The present study demonstrated that GATA4 was upregulated in children with acute lymphoblastic leukemia (ALL). Results from a number of functional experiments, including cell proliferation analysis, cell cycle analysis, cell apoptosis assay and Transwell migration and invasion analyses, have suggested that high expression of GATA4 may facilitate proliferation and metastasis, and suppress apoptosis in ALL cells. Chromatin immunoprecipitation assay and luciferase reporter assay revealed that GATA4 was a transcription factor that activated mouse double minute 2 homolog (MDM2) and B cell lymphoma 2 (BCL2) expression in ALL cells. BCL2 is a key anti‑apoptosis protein that was demonstrated to suppress cell apoptosis. In addition, GATA4 was revealed to regulate p53 through the transcriptional activation of MDM2, subsequently influencing cell cycle and apoptosis. Results from the present study suggested that GATA4 may be a key marker in ALL diagnosis and a potential target of molecular therapy.

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“…p62, an autophagic cargo protein, binds to endogenous autophagy substrates during autophagic lysosomal degradation. GATA4 acts as an activator of hepatoblastoma cell proliferation [18] ; after binding to p62, GATA4 is degraded through the autophagic lysosomal pathway [19] . Our results showed that p62 binds to c-Myc, causing c-Myc degradation through the lysosomal pathway ( Figure 5), which is consistent with [20] , but they did not discuss AMBRA1 causes the degradation of c-Myc by ubiquitin proteasome pathway or the autophagy-lysosomal pathway.…”

Section: Discussionmentioning

confidence: 99%

EBP50 suppresses the proliferation of MCF-7 human breast cancer cells via promoting Beclin-1/p62-mediated lysosomal degradation of c-Myc

et al. 2017

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c-Myc, a key activator of cell proliferation and angiogenesis, promotes the development and progression of breast cancer. Ezrin-radixin-moesin-binding phosphoprotein-50 (EBP50) is a multifunctional scaffold protein that suppresses the proliferation of breast cancer cells. In this study we investigated whether the cancer-suppressing effects of EBP50 resulted from its regulation of c-Myc signaling in human breast cancer MCF-7 cells in vitro and in vivo. We first found a significant correlation between EBP50 and c-Myc expression levels in breast cancer tissue, and demonstrated that EBP50 suppressed cell proliferation through decreasing the expression of c-Myc and its downstream proteins cyclin A, E and Cdc25A in MCF-7 cells. We further showed that EBP50 did not regulate c-Myc mRNA expression, but it promoted the degradation of c-Myc through the autophagic lysosomal pathway. Moreover, EBP50 promoted integration between c-Myc and p62, an autophagic cargo protein, triggering the autophagic lysosomal degradation of c-Myc. In EBP50-silenced MCF-7 cells, activation of autophagy by Beclin-1 promoted the degradation of c-Myc and inhibited cell proliferation. These results demonstrate that the EBP50/Beclin-1/p62/c-Myc signaling pathway plays a role in the proliferation in MCF-7 breast cancer cells: EBP50 stimulates the autophagic lysosomal degradation of c-Myc, thereby inhibits the proliferation of MCF-7 cells. Based on our results, promoting the lysosomal degradation of c-Myc might be a promising new strategy for treating breast cancer.

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GATA4 promotes hepatoblastoma cell proliferation by altering expression of miR125b and DKK3

Cited by 16 publications

References 42 publications

Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

GATA4 is highly expressed in childhood acute lymphoblastic leukemia, promotes cell proliferation and inhibits apoptosis by activating BCL2 and MDM2

EBP50 suppresses the proliferation of MCF-7 human breast cancer cells via promoting Beclin-1/p62-mediated lysosomal degradation of c-Myc

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