DCAF13 promotes triple-negative breast cancer metastasis by mediating DTX3 mRNA degradation

Liu, Jiazhe; Li, Hongchang; Mao, Anwei; Lu, Jingfeng; Liu, Weiyan; Qie, Jingbo; Pan, Gaofeng

doi:10.1080/15384101.2020.1859196

Cited by 29 publications

(41 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…DTX3 inhibits the proliferation and tumorigenicity of esophageal cancer cells and promotes the ubiquitination and degradation of Notch2 ( Ding et al, 2020 ). Furthermore, DTX3 acts as a tumor suppressor gene in triple-negative breast cancer and is expressed at a low level, which hinders its ubiquitination and degradation ability toward Notch4 and its ability to effectively inhibit triple-negative breast cancer metastasis ( Liu et al, 2020 ).…”

Section: Functions and Associated Molecular Mechanisms Of The Dtx Familymentioning

confidence: 99%

Functions and Molecular Mechanisms of Deltex Family Ubiquitin E3 Ligases in Development and Disease

Wang

Sun

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Ubiquitination is a posttranslational modification of proteins that significantly affects protein stability and function. The specificity of substrate recognition is determined by ubiquitin E3 ligase during ubiquitination. Human Deltex (DTX) protein family, which functions as ubiquitin E3 ligases, comprises five members, namely, DTX1, DTX2, DTX3, DTX3L, and DTX4. The characteristics and functional diversity of the DTX family proteins have attracted significant attention over the last decade. DTX proteins have several physiological and pathological roles and are closely associated with cell signal transduction, growth, differentiation, and apoptosis, as well as the occurrence and development of various tumors. Although they have been extensively studied in various species, data on structural features, biological functions, and potential mechanisms of action of the DTX family proteins remain limited. In this review, recent research progress on each member of the DTX family is summarized, providing insights into future research directions and potential strategies in disease diagnosis and therapy.

show abstract

Section: Functions and Associated Molecular Mechanisms Of The Dtx Familymentioning

confidence: 99%

Functions and Molecular Mechanisms of Deltex Family Ubiquitin E3 Ligases in Development and Disease

Wang

Sun

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…59 In addition, promoting the proteasomal degradation of N4ICD in CSCs by recovering the expression of E3 ubiquitin-ligase Fbxw7a or DTX3 was also confirmed effective in blocking Notch4 signal transduction and its oncogenic function. 5,41 The main challenge of the discussed treatment strategies is their potential pan-Notch inhibitory effect. GSIs are wellknown pan-Notch inhibitors that show serious adverse effects in clinical trials, such as gastrointestinal toxicity.…”

Section: Blocking Notch4 Signal Transductionmentioning

confidence: 99%

“…A recent study reported that Notch4 overexpression promotes BC cell invasion, which is induced by the RNA-binding protein (RBP) DCAF13, which inhibits the activation of the E3 ubiquitin-protein ligase DTX3 and prevents Notch4 degradation. 5 An in vitro experiment indicates that there is a positive crosstalk between Notch4 and EMT-promoting Stat3-MMP signaling in BC metastasis: N4ICD can physically interact with the EMT-promoting Stat3 protein to activate it in BC cells, which leads to the upregulation of MMP2 expression. Stat3 signaling, in turn, maintains the activation of Notch4 and N4ICD.…”

Section: Notch4 Signaling In Cancer Emt and Metastasismentioning

confidence: 99%

“…Finally, NICD undergoes proteasomal degradation induced by E3 ubiquitin-ligases such as FBXW7 and DTX3. [1][2][3][4][5] Aberrant Notch signaling has been discovered in many cancer types, and it is known to play unique roles during cancer occurrence and progression. [6][7][8][9][10] The gene encoding Notch4 protein is located on chromosome 6p21.32 (6: 32194843-32224067), and contains 31 exons.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Targeting Notch4 in Cancer: Molecular Mechanisms and Therapeutic Perspectives

Xiu¹,

Zeng²,

Shan³

et al. 2021

CMAR

View full text Add to dashboard Cite

The dysregulation of Notch signaling is found in many cancers and is closely related to cancer progression. As an important Notch receptor, abnormal Notch4 expression affects several tumor-cell behaviors, including stemness, the epithelial-mesenchymal transition, radio/chemoresistance and angiogenesis. In order to inhibit the oncogenic effects of Notch4 activation, several methods for targeting Notch4 signaling have been proposed. In this review, we summarize the known molecular mechanisms through which Notch4 affects cancer progression. Finally, we discuss potential Notch4-targeting therapeutic strategies as a reference for future research.

show abstract

“…RNA-binding proteins (RBPs) are critical regulators of gene expression by which involved in various aspects of RNA metabolism, such as splicing, modification, stability, and translation [5][6][7][8] . Growing number of studies have revealed that altered RNA metabolism due to dysfunction of RBP plays an important role in cancer progression, especially cancer cell metastasis 9,10 . Notably, dysregulated RBPs were also observed in HCC.…”

Section: Introductionmentioning

confidence: 99%

Ribosomal protein L23 drives the metastasis of hepatocellular carcinoma via upregulating MMP9

Chen

Fan

Yang

et al. 2021

Preprint

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths globally and tumor metastasis is one of the major causes of high mortality. To identify novel molecules contributing to HCC metastasis is critical to understanding the underlining mechanism of cancer metastasis. Here, combining the analyze based on published database and liver tissues from HCC patients, we identified that RNA binding protein L23 (RPL23) as a tumor metastasis driver in HCC. RPL23 was elevated in HCC and closely related to poor clinical outcomes. Furthermore, RPL23 depletion inhibited HCC cell proliferation, migration and invasion, while RPL23 overexpression promoted HCC cell metastasis. Mechanistically, RPL23 positively regulated MMP9 expression by stabilizing its mRNA. And increased MMP9 is involved in RPL23-mediated HCC metastasis. Importantly, RPL23 silencing reduced tumor growth and metastasis in vivo. In summary, we identified that RPL23 play an important role in HCC metastasis in an MMP9-dependent manner and may be a novel potential therapeutic target for HCC tumorigenesis and metastasis.

show abstract

DCAF13 promotes triple-negative breast cancer metastasis by mediating DTX3 mRNA degradation

Cited by 29 publications

References 32 publications

Functions and Molecular Mechanisms of Deltex Family Ubiquitin E3 Ligases in Development and Disease

Functions and Molecular Mechanisms of Deltex Family Ubiquitin E3 Ligases in Development and Disease

Targeting Notch4 in Cancer: Molecular Mechanisms and Therapeutic Perspectives

Ribosomal protein L23 drives the metastasis of hepatocellular carcinoma via upregulating MMP9

Contact Info

Product

Resources

About