MYH9 promotes cell metastasis <i>via</i> inducing Angiogenesis and Epithelial Mesenchymal Transition in Esophageal Squamous Cell Carcinoma

Yang, Bin; Liu, Huijuan; Bi, Yanghui; Chen, Cheng; Li, Guodong; Kong, Ping; Zhang, Ling; Shi, Ruyi; Zhang, Yunkui; Zhang, Rongsheng; Cheng, Xiaolong

doi:10.7150/ijms.46234

Cited by 23 publications

(16 citation statements)

References 30 publications

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“…In the initial study, MYH9 was reported as a tumor suppressor participating in the pathogenesis of squamous cell carcinoma 14 , 15 . However, some reversed studies showed that MYH9 functions as a potential oncogene in most tumors and promotes the tumor occurrence, metastasis and tumor stemness formation 16 - 19 , including esophageal squamous cell carcinoma and nasopharyngeal carcinoma 20 , 21 . These studies show the complexity and importance of MYH9 in tumor pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

ENKUR expression induced by chemically synthesized cinobufotalin suppresses malignant activities of hepatocellular carcinoma by modulating β-catenin/c-Jun/MYH9/USP7/c-Myc axis

Hou¹,

Li²,

Luo³

et al. 2022

Int. J. Biol. Sci.

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ENKUR plays a crucial role in lung and colorectal cancers. Chemically synthesized cinobufotalin (CB) showed its significant anti-cancer effect in nasopharyngeal carcinoma. However, the roles of ENKUR and CB along with their correlation are still unknown in hepatocellular carcinoma (HCC). In this study, ENKUR expression in HCC tissue and cells were detected. The relationship between ENKUR expression and clinical pathology was also assessed. In vivo and in vitro experiments were conducted to explore the effects and molecular basis of ENKUR and CB in HCC. ENKUR expression was correlated with HCC progression and patient prognosis. Furthermore, ENKUR could inhibit tumor proliferation, metastasis, and sorafenib resistance in HCC. Mechanistic studies showed that ENKUR or its Enkurin domain could bind to MYH9 and decrease its expression by binding to β-catenin and inhibiting its nuclear transfer, thus decreasing c-Jun level. Low expression of MYH9 suppressed recruitment of deubiquitination enzyme USP7, promoting degradation of the c-Myc. Therefore, cell cycle and EMT signals were suppressed. CB as a safe and effective anti-cancer compound up-regulates the expression of ENKUR via inhibiting PI3K/AKT/c-Jun-mediated transcription suppression. These findings show that ENKUR induced by CB antagonizes β-catenin/c-Jun/MYH9/USP7 pathway, thus increasing c-Myc ubiquitin degradation and finally suppressing cell cycle and EMT signals.

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Section: Introductionmentioning

confidence: 99%

ENKUR expression induced by chemically synthesized cinobufotalin suppresses malignant activities of hepatocellular carcinoma by modulating β-catenin/c-Jun/MYH9/USP7/c-Myc axis

Hou¹,

Li²,

Luo³

et al. 2022

Int. J. Biol. Sci.

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“…MYH9 is a widespread cytoplasmic myosin and is involved in the translocation of the skeleton proteins ( 54 ). Moreover, some studies showed that MYH9 was upregulated in gastric cancer, which could promote the transcription of β-catenin ( 55 ) and could be upregulated in esophageal squamous cell carcinoma (ESCC) facilitating cell metastasis ( 56 ). Also, MYH9 could bind with and degrade GSK3β through ubiquitin, therefore β-catenin was downregulated to induce the epithelial-mesenchymal transition in hepatocellular carcinoma ( 57 ).…”

Section: Discussionmentioning

confidence: 99%

Dynamics and Functional Interplay of Nonhistone Lysine Crotonylome and Ubiquitylome in Vascular Smooth Muscle Cell Phenotypic Remodeling

Cao

Chen

et al. 2022

Front. Cardiovasc. Med.

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BackgroundThe crotonylation of histones is discovered of late as one of the post-translational modifications (PTMs) that can regulate gene expression. However, the function of crotonylation on nonhistone proteins in vascular smooth muscle cells (VSMCs) is unclear. Here, we aim to find the cellular characteristics of crotonylated nonhistone proteins and the cross talk with ubiquitinated proteins in VSMC phenotypic remodeling using the modified omics and proteomic analysis.MethodsWe performed the modified omics and proteomic analysis of VSMCs before and after the stimulation with platelet-derived growth factor-BB (PDGF-BB). The crotonylated and ubiquitinated pan-antibody was used to enrich proteins and then subjected to a high-throughput mass spectrometry analysis. The enrichment analysis was performed within differentially modified proteins in regard to GO terms, KEGG, and protein domains.ResultsAs a result, there were 2,138 crotonylation sites in 534 proteins and 1,359 ubiquitination sites corresponding to 657 proteins. These crotonylated proteins detected after PDGF-BB stimulation might be involved in various vital cellular pathways and carry out important functions in VSMCs. Some of them closely took part in significant physiological processes of VSMC phenotypic remodeling, including glycolysis/gluconeogenesis, vascular smooth muscle contraction, and the PI3K-Akt signaling pathway. Furthermore, the KEGG pathway enrichment analysis showed the involvement of ubiquitinated proteins in the physiological processes of VSMC phenotypic remodeling, including glycolysis/gluconeogenesis, vascular smooth muscle contraction, RAS signaling pathway, or the PI3K-Akt signaling pathway. A cross talk analysis showed that there were 199 sites within the 177 proteins modified by crotonylation and ubiquitination simultaneously. Protein–protein interaction (PPI) network analysis indicated that crotonylated and ubiquitinated proteins play an important role in cellular bioprocess commonly and possibly have a synergistic effect.ConclusionIn summary, our bioinformatics analysis shows that the crotonylation and ubiquitination of nonhistone proteins play an essential role in VSMC phenotypic transformation induced by PDGF-BB stimulation. The cross talk between crotonylation and ubiquitination in glycolysis is possibly a novel mechanism during VSMC phenotypic remodeling.

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“…Non-muscle myosin heavy chain9(MYH9) is widely expressed in various tissues and cells. MYH9 is abnormally highly expressed in esophageal squamous cell carcinoma 17 , breast cancer 18 , epithelial ovarian cancer 19 and acute myeloid leukemia 20 and is associated with poor prognosis. Researchers report that MYH9 degrades GSK3β protein through TRAF6-induced ubiquitination, enhancing the stem cell characteristics, migration, invasion, growth and sorafenib resistance of HCC cells 21 .…”

Section: Discussionmentioning

confidence: 99%

Identification of TLN1 as a prognostic biomarker to effect cell proliferation and differentiation in Acute Myeloid Leukemia

Zheng

Cui

Cui³

et al. 2022

Preprint

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The protein Talin1 encoded by the TLN1 gene is a focal adhesion-related protein that binds to various cytoskeletal proteins and plays an important role in cell adhesion and movement. Recent studies have shown that it is overexpressed in prostate cancer, liver cancer, and oral squamous cell carcinoma, and is closely related to tumor progression and metastasis. This study integrated bioinformatics and functional analysis to reveal the prognosis and potential functions of TLN1 in AML. The results showed that the expression level of TLN1 was abnormally increased in AML and localized in the cell membrane and cytoplasm, which is a significant prognostic indicator of overall survival(OS). Enrichment analysis of related genes showed that TLN1 is related to neutrophil mediated immunity, neutrophil activation and may regulate important signal pathways in hematological tumors including tyrosine kinase receptor, FLT3 and PIK3/AKT. The PPI network shows that TLN1 and MYH9 may be involved in the process of AML tumors together with PIP5K1C, ROCK1, S100A4, MY01A and WAC. Immune infiltration analysis explains that TLN1 is associated with multiple immune cells and may be an important immune marker in AML. Furthermore, molecular biology experiments confirmed that TLN1 is related to the proliferation, differentiation and cycle of AML cells. Silencing TLN1 can inhibit the proliferation of AML cells and promote differentiation through the Talin1/P-AKT/CREB signaling pathway.

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MYH9 promotes cell metastasis via inducing Angiogenesis and Epithelial Mesenchymal Transition in Esophageal Squamous Cell Carcinoma

Cited by 23 publications

References 30 publications

ENKUR expression induced by chemically synthesized cinobufotalin suppresses malignant activities of hepatocellular carcinoma by modulating β-catenin/c-Jun/MYH9/USP7/c-Myc axis

ENKUR expression induced by chemically synthesized cinobufotalin suppresses malignant activities of hepatocellular carcinoma by modulating β-catenin/c-Jun/MYH9/USP7/c-Myc axis

Dynamics and Functional Interplay of Nonhistone Lysine Crotonylome and Ubiquitylome in Vascular Smooth Muscle Cell Phenotypic Remodeling

Identification of TLN1 as a prognostic biomarker to effect cell proliferation and differentiation in Acute Myeloid Leukemia

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