DAXX inhibits cancer stemness and epithelial–mesenchymal transition in gastric cancer

Wu, Chaofan; Ding, Hui; Wang, Shuochen; Li, Yangxin; Liu, Song Bai; Wang, Xiaoxiao; Jian, Zheng; Xue, Ting; Amin, Hesham M.; Song, Yanyu; Zhou, Jin

doi:10.1038/s41416-020-0800-3

Cited by 21 publications

(25 citation statements)

References 24 publications

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“…Deciphered using the framework developed previously, it has been widely known that EMT and cancer stemness are closely related to the tumor progression and metastasis in various types of cancer cells ( Pang et al, 2017 ; Matsuyama et al, 2019 ; Park et al, 2019a ; Wu et al, 2020 ). Thus, we speculated that ENC1 might be involved in the EMT process and stemness in CRC cells.…”

Section: Resultsmentioning

confidence: 99%

ENC1 Facilitates Colorectal Carcinoma Tumorigenesis and Metastasis via JAK2/STAT5/AKT Axis-Mediated Epithelial Mesenchymal Transition and Stemness

Cui

Yang

Bai

et al. 2021

Front. Cell Dev. Biol.

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Ectodermal neural cortex 1 (ENC1) is an actin-binding protein and has been known to be upregulated in several cancers, but the molecular mechanisms through which it contributes to the pathology of CRC have largely been elusive. We utilized data mining and validated the aberrant expression of ENC1, following which phenotypic traits of malignancy were assessed in vitro. Ruxolitinib was used as a surrogate to compare the effects of ENC1 expression and silencing on the JAK-STAT-AKT pathway. In vivo models were employed to confirm the in vitro observations. Computation analysis, strengthened by in situ and in vitro data, confirmed the overexpression of ENC1 in CRC and predicted a poor prognosis, while enhanced cell proliferation, invasion, migration, EMT, and stemness were associated with ENC1 overexpression. Silencing of ENC1 downregulated the phenotypes. Additionally, silencing of ENC1 significantly reduced the activation of JAK2 and consequent activation of STAT5 and AKT comparable to ruxolitinib inhibition of JAK2. Silencing of ENC1 resulted in lesser tumor volumes and fewer numbers of tumors, in vivo. These data suggest that ENC1 induces CRC through the JAK2-STAT5-AKT axis. ENC1 is a suitable diagnostic marker for CRC detection, and ENC1 targeting therapies may suppress CRC progression.

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Section: Resultsmentioning

confidence: 99%

ENC1 Facilitates Colorectal Carcinoma Tumorigenesis and Metastasis via JAK2/STAT5/AKT Axis-Mediated Epithelial Mesenchymal Transition and Stemness

Cui

Yang

Bai

et al. 2021

Front. Cell Dev. Biol.

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“…Type 3 is related to tumor progression and metastasis 29 . Many clinical studies have determined that many different organ epithelial cells are transformed into myo broblasts and broblast phenotypes through EMT leading to tissue brosis, such as renal tubules, lens epithelial cells, alveolar epithelial cells, and peritoneal mesothelial cells [30][31][32] .…”

Section: Discussionmentioning

confidence: 99%

LINC01272 Activates Epithelial-Mesenchymal Transition Through miR-153-5p in Crohn’s Disease

Fang

Xia

et al. 2021

Preprint

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Background: Long non-coding RNAs (lncRNAs) have different functions in different diseases. There is seldom research on the functions of lncRNAs in Crohn’s disease (CD). By RNA-seq technology, we identify a lncRNA associated with Crohn's disease. However, the mechanism of lncRNA regulation remains unknown. This study aimed to determine the association of LINC01272 with epithelial cell-mesenchymal transition and the underlined mechanism in CD.Methods: RNA is detected by qRT-PCR. Interaction of protein and RNA was determined by RNA binding protein immunoprecipitation. Luciferase reporter assays were used to detect the targeted miRNA of LINC01272. Tissue fibrosis was observed by Masson and HE staining. The protein expression is determined by western blot and immunofluorescence. Results: LINC01272 was highly expressed in patients with CD. Knockdown of LINC01272 inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT). Additionally, LINC01272 regulated TGF-β1 induced EMT by miR-153-5p axis and knockdown of LINC01272 inhibited EMT in the CD mice in vivo. Conclusion: LINC01272 activated epithelial-mesenchymal transition through miR-153-5p in CD.

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“…For example, DAXX is overexpressed in many types of cancer such as prostate cancer ( 118 , 120 , 130 ), ovarian cancer ( 121 , 122 ), gastric cancer ( 123 ), and gliomas ( 14 ). DAXX is downregulated in advanced gastric cancer ( 125 ) and human colon adenocarcinoma cells ( 126 , 127 ), lung cancer ( 128 ), and PanNETs ( 129 ). One study suggests that DAXX binds to anaphase promoting complex (APC) coactivators Cdc20 and Cdh1 to inhibit the degradation of APC, thereby promoting chromosome instability during prostate cancer development ( 118 ).…”

Section: Daxx and Cancermentioning

confidence: 99%

“…The upregulation of DAXX in gastric cancer cells inhibited proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). DAXX overexpression inhibited the growth of gastric cancer through downregulating snail family transcriptional repressor 3 (SNAI3), a key inducer of EMT, by recruiting HDAC-1 into the nucleus ( 125 ). Similarly, a study lead by Tzeng et al.…”

Section: Daxx and Cancermentioning

confidence: 99%

Dynamic Activity of Histone H3-Specific Chaperone Complexes in Oncogenesis

Wen

Chen

2022

Front. Oncol.

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Canonical histone H3.1 and variant H3.3 deposit at different sites of the chromatin via distinct histone chaperones. Histone H3.1 relies on chaperone CAF-1 to mediate replication-dependent nucleosome assembly during S-phase, while H3.3 variant is regulated and incorporated into the chromatin in a replication-independent manner through HIRA and DAXX/ATRX. Current literature suggests that dysregulated expression of histone chaperones may be implicated in tumor progression. Notably, ectopic expression of CAF-1 can promote a switch between canonical H3.1 and H3 variants in the chromatin, impair the chromatic state, lead to chromosome instability, and impact gene transcription, potentially contributing to carcinogenesis. This review focuses on the chaperone proteins of H3.1 and H3.3, including structure, regulation, as well as their oncogenic and tumor suppressive functions in tumorigenesis.

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DAXX inhibits cancer stemness and epithelial–mesenchymal transition in gastric cancer

Cited by 21 publications

References 24 publications

ENC1 Facilitates Colorectal Carcinoma Tumorigenesis and Metastasis via JAK2/STAT5/AKT Axis-Mediated Epithelial Mesenchymal Transition and Stemness

ENC1 Facilitates Colorectal Carcinoma Tumorigenesis and Metastasis via JAK2/STAT5/AKT Axis-Mediated Epithelial Mesenchymal Transition and Stemness

LINC01272 Activates Epithelial-Mesenchymal Transition Through miR-153-5p in Crohn’s Disease

Dynamic Activity of Histone H3-Specific Chaperone Complexes in Oncogenesis

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