ZNF326 promotes a malignant phenotype of breast cancer by interacting with DBC1

Yu, Xinmiao; Wang, Minghao; Han, Qiang; Zhang, Xiupeng; Mao, Xiaoyun; Wang, Xu; Li, Xiaoying; Ma, Wei; Jin, Feng

doi:10.1002/mc.22898

Cited by 10 publications

(7 citation statements)

References 30 publications

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“…However, taken together, our results particularly with increased AKT1 signaling and anchorage independence assay show that DBC1 over-expression in U2OS cells promotes oncogenic pathways. These results are consistent with some recent reports also suggesting the oncogenic role of DBC1 (21)(22)(23).…”

Section: Energy Deficit Is Critical For the Induction Of Mitotic Arresupporting

confidence: 94%

LKB1 negatively regulates AKT1 signaling via DBC1 and TRB3

Sarwar

Bhat

Gillani

et al. 2019

Preprint

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DBC1 plays a critical role in various cellular functions notably cell proliferation, transcription, histone modification and adipogenesis. Current reports about the role of DBC1 in tumorigenesis areparadoxical and designate DBC1 both as a tumor suppressor or an oncogene. Here, using small T antigen of polyoma virus (PyST) as a tool, we have delineated a signaling mechanism that connects LKB1 to AKT1 via DBC1. We report that PyST associates with DBC1 and leads to its down- regulation. Our results also show that PyST expression promotes LKB1 activation which in turn leads to in the downregulation of DBC1 protein. Absence of DBC1 results in transcriptional upregulationand consequently enhanced protein levels of TRB3. TRB3 sequesters AKT1, and consequently the phosphorylation and activity of AKT1 is compromised. This ultimately results in inactivation of prosurvival pathways triggered via AKT1 signaling. Our studies thus provide an insight into a signaling pathway that connects LKB1, DBC1, TRB3 and AKT1.Running title: DBC1 regulates signaling from LKB1 to AKT.

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Section: Energy Deficit Is Critical For the Induction Of Mitotic Arresupporting

confidence: 94%

LKB1 negatively regulates AKT1 signaling via DBC1 and TRB3

Sarwar

Bhat

Gillani

et al. 2019

Preprint

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“…Furthermore, we recover the link to the interaction of MALAT1 with DBC1 [22]. While we did not directly enrich DBC1 as an interactor of Malat1, we identified Zfp326 that interacts directly with DBC1 [30,31]. We also detected binding of Elavl1 (also known as HuR) to MALAT1 previously reported to form a complex that represses transcription [32].…”

Section: Discussionmentioning

confidence: 50%

Quantitative Proteomics to Identify Nuclear RNA-Binding Proteins of Malat1

Scherer

Levin

Butter

et al. 2020

IJMS

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The long non-coding RNA Malat1 has been implicated in several human cancers, while the mechanism of action is not completely understood. As RNAs in cells function together with RNA-binding proteins (RBPs), the composition of their RBP complex can shed light on their functionality. We here performed quantitative interactomics of 14 non-overlapping fragments covering the full length of Malat1 to identify possible nuclear interacting proteins. Overall, we identified 35 candidates including 14 already known binders, which are able to interact with Malat1 in the nucleus. Furthermore, the use of fragments along the full-length RNA allowed us to reveal two hotspots for protein binding, one in the 5 -region and one in the 3 -region of Malat1. Our results provide confirmation on previous RNA-protein interaction studies and suggest new candidates for functional investigations.

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“…We found that lncRNA 604 binds to the nuclear transcription factor ZNF326 and could positively regulate its expression. Furthermore, we demonstrated that ZNF326 could accelerate the occurrence of EMT ( 29 , 30 ). Therefore, we also concluded that lncRNA 604 could promote the metastasis of CRC by regulating ZNF326 in the nucleus.…”

Section: Discussionmentioning

confidence: 79%

LncRNA-ENST00000543604 exerts a tumor-promoting effect via miRNA 564/AEG-1 or ZNF326/EMT and predicts the prognosis of and chemotherapeutic effect in colorectal cancer

et al. 2022

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ObjectivesColorectal cancer(CRC) is a common malignant tumor. Recent studies have found that lncRNAs play an important role in the occurrence and development of colorectal cancer.MethodsBased on high-throughput sequencing results of fresh CRC tissues and adjacent tissues, we identified lncRNA-ENST00000543604 (lncRNA 604) as the research object by qRT-PCR in CRC tissues and cells. We explored the mechanism of lncRNA 604 action by using luciferin reporter, qRT-PCR and Western blot assays. Kaplan-Meier survival analysis and a Cox regression model were used to analyze the correlation of lncRNA 604 and its regulatory molecules with the prognosis of and chemotherapy efficacy in CRC patients.ResultsIn this study, we found that the expression levels of lncRNA 604 were increased in CRC. LncRNA 604 could promote CRC cell proliferation and metastasis through the miRNA 564/AEG-1 or ZNF326/EMT signaling axis in vivo and in vitro. LncRNA 604 could predict the prognosis of CRC and was an independent negative factor. LncRNA 604 exerted a synergistic effect with miRNA 564 or ZNF326 on the prognosis of CRC. LncRNA 604 could improve chemoresistance by increasing the expression of AEG-1, NF-κB, and ERCC1.ConclusionsOur study demonstrated that lncRNA 604 could promote the progression of CRC via the lncRNA 604/miRNA 564/AEG-1/EMT or lncRNA 604/ZNF326/EMT signaling axis. LncRNA 604 could improve chemoresistance by increasing drug resistance protein expression.

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ZNF326 promotes a malignant phenotype of breast cancer by interacting with DBC1

Cited by 10 publications

References 30 publications

LKB1 negatively regulates AKT1 signaling via DBC1 and TRB3

LKB1 negatively regulates AKT1 signaling via DBC1 and TRB3

Quantitative Proteomics to Identify Nuclear RNA-Binding Proteins of Malat1

LncRNA-ENST00000543604 exerts a tumor-promoting effect via miRNA 564/AEG-1 or ZNF326/EMT and predicts the prognosis of and chemotherapeutic effect in colorectal cancer

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