N3ICD with the transmembrane domain can effectively inhibit EMT by correcting the position of tight/adherens junctions

Tan, Junyu; Zhang, Xixun; Xiao, Wenjun; Liu, Xiong; Li, Chun; Guo, Yuxian; Xiong, Wei; Li, Yaochen

doi:10.1080/19336918.2019.1619958

Cited by 6 publications

(8 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All cells were routinely tested for the absence of mycoplasma using a Mycoplasma Detection Kit (Bitool, China). All cells were cultured in complete medium as our previously described method [33]. We constructed a breast cancer cell line (4T-1-luc) that stably knocks out HDAC2 (HDAC2-KO) and nontargeted control (WT) cell lines using CRISPR/Cas9 technology, as we described previously [27].…”

Section: Cell Line Culture Antibodies and Reagentsmentioning

confidence: 99%

Histone deacetylase 2 knockout suppresses immune escape of triple-negative breast cancer cells via downregulating PD-L1 expression

Xiong

Lin

et al. 2021

Cell Death Dis

Self Cite

View full text Add to dashboard Cite

The PD-L1 overexpression is an important event of immune escape and metastasis in triple-negative breast cancer (TNBC), but the molecular mechanism remains to be determined. Interferon gamma (IFNγ) represents a major driving force behind PD-L1 expression in tumor microenvironment, and histone deacetylase 2 (HDAC2) is required for IFN signaling. Here, we investigated the regulation of HDAC2 on the IFNγ-induced PD-L1 expression in TNBC cells. We found the HDAC2 and PD-L1 expression in TNBC was significantly higher than that in non-TNBC, and HDAC2 was positively correlated with PD-L1 expression. HDAC2 promoted PD-L1 induction by upregulating the phosphorylation of JAK1, JAK2, and STAT1, as well as the translocation of STAT1 to the nucleus and the recruitment of STAT1 to the PD-L1 promoter. Meanwhile, HDAC2 was recruited to the PD-L1 promoter by STAT1, and HDAC2 knockout compromised IFNγ-induced upregulation of H3K27, H3K9 acetylation, and the BRD4 recruitment in PD-L1 promoter. In addition, significant inhibition of proliferation, colony formation, migration, and cell cycle of TNBC cells were observed following knockout of HDAC2 in vitro. Furthermore, HDAC2 knockout reduced IFNγ-induced PD-L1 expression, lymphocyte infiltration, and retarded tumor growth and metastasis in the breast cancer mouse models. This study may provide evidence that HDAC2 promotes IFNγ-induced PD-L1 expression, suggesting a way for enhanced antitumor immunity when targeting the HDAC2 in TNBC.

show abstract

Section: Cell Line Culture Antibodies and Reagentsmentioning

confidence: 99%

Histone deacetylase 2 knockout suppresses immune escape of triple-negative breast cancer cells via downregulating PD-L1 expression

Xiong

Lin

et al. 2021

Cell Death Dis

Self Cite

View full text Add to dashboard Cite

show abstract

“…EMT promotes the transformation of immobile epithelial cells into motile mesenchymal cells, enhancing the metastatic properties [69,70]. Further, adherens and tight junctions become impaired, resulting in a mesenchymal phenotype [12,[71][72][73]. Altered E-and N-cadherin levels and the following β-catenin activation promote the expression of many tumor-associated proteins, including cyclin D1, CD44, or c-MYC [54,[74][75][76][77][78][79].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Baj

Korona-Głowniak

Forma

et al. 2020

Cells

124

View full text Add to dashboard Cite

Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world's population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial-mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial-mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

show abstract

“…The authors showed that the Fos-related antigen 1 protein, a regulator involved in cell proliferation, differentiation, and transformation and EMT promotion, is negatively regulated by Notch3 in tumor cells, thus revealing the onco-suppressive role of the receptor [ 172 ] . In keeping with these findings, it has been observed that Notch3 may negatively regulate EMT [ 173 - 176 ] , by acting, at least in part, via GATA-3 induction in BC cells [ 174 ] . This suggest that the involvement of Notch signaling is complex and context-dependent and further investigations are needed.…”

Section: Notch Signaling and Emtmentioning

confidence: 68%

Notch signaling in female cancers: a multifaceted node to overcome drug resistance

Giuli¹,

Mancusi²,

Giuliani³

et al. 2021

CDR

View full text Add to dashboard Cite

Drug resistance is one of the main challenges in cancer therapy, including in the treatment of female-specific malignancies, which account for more than 60% of cancer cases among women. Therefore, elucidating the underlying molecular mechanisms is an urgent need in gynecological cancers to foster novel therapeutic approaches. Notably, Notch signaling, including either receptors or ligands, has emerged as a promising candidate given its multifaceted role in almost all of the hallmarks of cancer. Concerning the connection between Notch pathway and drug resistance in the afore-mentioned tumor contexts, several studies focused on the Notchdependent regulation of the cancer stem cell (CSC) subpopulation or the induction of the epithelial-tomesenchymal transition (EMT), both features implicated in either intrinsic or acquired resistance. Indeed, the present review provides an up-to-date overview of the published results on Notch signaling and EMT-or CSCdriven drug resistance. Moreover, other drug resistance-related mechanisms are examined such as the involvement of the Notch pathway in drug efflux and tumor microenvironment. Collectively, there is a long way to go before every facet will be fully understood; nevertheless, some small pieces are falling neatly into place. Overall, the main aim of this review is to provide strong evidence in support of Notch signaling inhibition as an effective strategy to evade or reverse resistance in female-specific cancers.

show abstract

N3ICD with the transmembrane domain can effectively inhibit EMT by correcting the position of tight/adherens junctions

Cited by 6 publications

References 49 publications

Histone deacetylase 2 knockout suppresses immune escape of triple-negative breast cancer cells via downregulating PD-L1 expression

Histone deacetylase 2 knockout suppresses immune escape of triple-negative breast cancer cells via downregulating PD-L1 expression

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Notch signaling in female cancers: a multifaceted node to overcome drug resistance

Contact Info

Product

Resources

About