Silencing of GATA6 Suppresses SW1990 Pancreatic Cancer Cell Growth In Vitro and Up-Regulates Reactive Oxygen Species

Chen, Wenbo; Huang, Fengting; Zhuang, Yanyan; Tang, Jian; Zhuang, Xiaohong; Cheng, Wenjie; Gu, Zhong Ze; Zhang, Shineng

doi:10.1007/s10620-013-2752-4

Cited by 10 publications

(10 citation statements)

References 31 publications

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“…In contrast, a tumor suppressive role of GATA6 in cetuximab resistance was demonstrated by decreasing the expression of MIR100HG 26 . Similarly, in PDAC, GATA6 was amplified in a subset of pancreatic tumors, and overexpression of GATA6 increased pancreatic cancer proliferation 27,28 . However, the classic PDAC subtype, which showed a better outcome, had a relatively high expression of GATA6, and GATA6 was proven to be a suppressor in the process of PDAC metastasis 6,29 .…”

Section: Discussionmentioning

confidence: 95%

GATA6 suppresses migration and metastasis by regulating the miR-520b/CREB1 axis in gastric cancer

Líu

Sun

et al. 2019

Cell Death Dis

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Transcription factors (TFs) and microRNAs (miRNAs) are tightly linked to each other in tumor development and progression, but their interactions in gastric cancer (GC) metastasis remain elusive. Here we report a novel suppressive role of GATA6 in inhibiting GC metastasis by transactivating miR-520b. We found that GATA6 expression was significantly downregulated in metastatic GC cells and tissues and that its downregulation was correlated with a poor GC prognosis. Overexpression of GATA6 suppressed GC cell migration, invasion and metastasis both in vitro and in vivo. Luciferase reporter assays and chromatin immunoprecipitation assays demonstrated that miR-520b is a direct transcriptional target of GATA6. Moreover, miR-520b expression was positively correlated with GATA6 expression in GC tissues, and ectopic expression of miR-520b inhibited the migration and invasion of GC cells. Furthermore, cAMP responsive element binding protein 1 (CREB1) was identified as a direct and functional target of miR-520b, and GATA6 could suppress GC cell migration and metastasis via miR-520b-mediated repression of CREB1. Downregulation of GATA6 and miR-520b may partly account for the overexpression of CREB1 in GC. In conclusion, our results provide novel insight into the TF-miRNA regulatory network involved in GC metastasis. Targeting the GATA6/miR-520b/CREB1 axis may be an effective approach for GC treatment.

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Section: Discussionmentioning

confidence: 95%

GATA6 suppresses migration and metastasis by regulating the miR-520b/CREB1 axis in gastric cancer

Líu

Sun

et al. 2019

Cell Death Dis

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“…This suggests that RNA interference methods for GATA6 may be an effective new method for the treatment of PC. 78 However, the role of GATA6 gene expression levels in PC may be more complex than reported in previous studies. A high GATA6 copy number is significantly associated with better outcomes in patients with PDAC.…”

Section: Gata6 and Pancreatic Cancermentioning

confidence: 83%

“…Silencing GATA6 by RNA interference can inhibit the proliferation of the SW1990 PC cell line and increase apoptosis and enhance the expression of reactive oxygen species. This suggests that RNA interference methods for GATA6 may be an effective new method for the treatment of PC . However, the role of GATA6 gene expression levels in PC may be more complex than reported in previous studies.…”

Section: Gata6 and Human Cancersmentioning

confidence: 87%

Multiple roles and regulatory mechanisms of the transcription factor GATA6 in human cancers

Sun

Yan

2019

Clinical Genetics

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Cancer is a common type of non-communicable disease, and its morbidity and mortality are rapidly increasing. It is expected to become the largest obstacle to the promotion of global human health in the future. Some transcription factors that play important regulatory roles in embryogenesis and subsequent tissue maintenance can be selectively amplified during tumorigenesis. Due to its high expression in the embryonic endoderm and mesoderm, GATA6 plays a crucial role in the normal development of early human heart, lung, digestive system, adrenal glands, breasts, ovaries, retina, skin, and nervous system. Up to now, overexpression of the GATA6 gene has been shown to play an important role in several cancers, including lung cancer, digestive system tumors, breast cancer, and ovarian cancer. However, the human body is a complex organism, which causes the transcription factor GATA6 to have multiple roles in cancer. In this review, we summarize the multiple roles of transcription factor GATA6 in various cancers and its regulatory mechanisms. The aim is to better understand the relationship between GATA6 gene expression and cancer development and to provide new insights for exploring potential therapeutic targets.

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“…been reported that genomic rearrangements in PDACs frequently include amplification of the GATA6 gene which, accordingly, has been found to be over-expressed [57,58]. Conversely, silencing of this gene has resulted in the inhibition of pancreatic cancer cell growth [59]. A possible underlying mechanism may be a GATA6mediated induction of the Wnt signalling pathway [60].…”

Section: Discussionmentioning

confidence: 99%

Identification of candidate miRNA biomarkers for pancreatic ductal adenocarcinoma by weighted gene co-expression network analysis

Giulietti¹,

Occhipinti²,

Principato³

et al. 2017

Cell Oncol.

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Silencing of GATA6 Suppresses SW1990 Pancreatic Cancer Cell Growth In Vitro and Up-Regulates Reactive Oxygen Species

Abstract: These results suggest that the RNA interference approach against GATA6 may be an effective therapeutic approach for treatment of pancreatic cancer.

Cited by 10 publications

References 31 publications

GATA6 suppresses migration and metastasis by regulating the miR-520b/CREB1 axis in gastric cancer

GATA6 suppresses migration and metastasis by regulating the miR-520b/CREB1 axis in gastric cancer

Multiple roles and regulatory mechanisms of the transcription factor GATA6 in human cancers

Identification of candidate miRNA biomarkers for pancreatic ductal adenocarcinoma by weighted gene co-expression network analysis

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