MTA3 regulates malignant progression of colorectal cancer through Wnt signaling pathway

Jiao, Taiwei; Li, Yue; Gao, Tong; Zhang, Yining; Feng, Mingliang; Liu, Mengyuan; Zhou, Huan; Sun, Mingjun

doi:10.1177/1010428317695027

Cited by 15 publications

(5 citation statements)

References 23 publications

(27 reference statements)

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“…Then, it was found that the emodin/MTA3 axis play a crucial role in regulating cardiac fibrosis. This is consistent with the recognized role of MTA3 in regulating a variety of cellular events ( Jiao et al., 2017 ). As a transcription factor, MTA3 becomes a cancer suppressor by inhibiting the proliferation, invasion, and migration of cancer cells ( Ma et al., 2016 ).…”

Section: Targets and Studies Of Emodin Against Anti-cardiovascular DIsupporting

confidence: 91%

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Gao

Pang

et al. 2020

Front. Pharmacol.

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Emodin is a natural occurring anthraquinone derivative isolated from roots and barks of numerous plants, molds, and lichens. It is found to be an active ingredient in different Chinese herbs including Rheum palmatum and Polygonam multiflorum, and it is a pleiotropic molecule with diuretic, vasorelaxant, anti-bacterial, anti-viral, antiulcerogenic, anti-inflammatory, and anti-cancer effects. Moreover, emodin has also been shown to have a wide activity of anti-cardiovascular diseases. It is mainly involved in multiple molecular targets such as inflammatory, anti-apoptosis, anti-hypertrophy, antifibrosis, anti-oxidative damage, abnormal, and excessive proliferation of smooth muscle cells in cardiovascular diseases. As a new type of cardiovascular disease treatment drug, emodin has broad application prospects. However, a large amount of evidences detailing the effect of emodin on many signaling pathways and cellular functions in cardiovascular disease, the overall understanding of its mechanisms of action remains elusive. In addition, by describing the evidence of the effects of emodin in detail, the toxicity and poor oral bioavailability of mice have been continuously discovered. This review aims to describe a timely overview of emodin related to the treatment of cardiovascular disease. The emphasis is to summarize the pharmacological effects of emodin as an anticardiovascular drug, as well as the targets and its potential mechanisms. Furthermore, the treatment of emodin compared with conventional cardiovascular drugs or target inhibitors, the toxicity, pharmacokinetics and derivatives of emodin were discussed.

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Section: Targets and Studies Of Emodin Against Anti-cardiovascular DIsupporting

confidence: 91%

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Gao

Pang

et al. 2020

Front. Pharmacol.

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“…The study suggests an abnormally high expression of MTA2 in CRC tissue and MTA2 is associated with prognosis CRC (25). Additionally, Jiao et al have revealed MTA3 overexpression contributes to cell proliferation, invasion, migration, and cell cycle progression of CRC cells (26). Combined with our findings that ZNF217 knockdown could significantly reduce the expressions of MTA2 and MTA3, we inferred that ZNF217 might contribute to CRC carcinogenesis and development by combining its zinc finger domain to the NuRD complex region of MTA2/MTA3.…”

Section: Effects Of Znf217 Knockdown On Mta2 Mta3 Snai1 and E-cadherin Proteins Expression Levelssupporting

confidence: 83%

lncRNA PCAT1 might coordinate ZNF217 to promote CRC adhesion and invasion through regulating MTA2/MTA3/Snai1/E-cadherin signaling

Zhang

Zhu

Han

et al. 2022

Cell Mol Biol (Noisy-le-grand)

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LncRNA prostate cancer-associated transcript 1 (PCAT1) is a well-known oncogene, but the mechanisms of exosomes PCAT1 in colorectal cancer (CRC) remain largely unknown. Thus, the mechanisms of exosomes lncRNA PCAT1 were investigated. The expressions of exosomes lncRNA PCAT1 in tissues from stage 0-I and stage II-III CRC patients, and intestinal epithelial cell line FHC and two CRC cell lines, HT29 and HCT8 were measured by real-time quantitative PCR. The effects of lncRNA PCAT1 on adhesion and invasion of two CRC cell lines were investigated by cell-matrix adhesion and transwell assays. In addition, the target of PCAT1 (ZNF217) was validated using an RNA immune precipitation assay. Finally, the protein levels of MTA2, MTA3, SNAI1, and E-cadherin in normal participants, stage 0-I and stage II-III CRC patients, as well as two cell lines with stable ZNF217 knockdown were investigated by western blotting. The plasma exosomal lncRNA PCAT1 was found to be significantly increased in the CRC tissues and cell lines. In addition, lncRNA PCAT1 knockdown significantly inhibited the adhesion and invasion of HT29 and HCT8 cells. RIP assay results showed lncRNA PCAT1 could target ZNF217, and downregulation of lncRNA PCAT1 could decrease the protein expressions of ZNF217 in two CRC cells lines. Moreover, ZNF217 knockdown significantly decreased MTA2, MTA3, and SNAI1 expressions, but increased E-cadherin expressions in both CRC cells lines. Exosomal lncRNA PCAT1 can promote the adhesion and invasion of CRC cells, and PCAT1 overexpression may lead to ZNF217 upregulation that regulates EMT-related MTA2/MTA3/Snai1/E-cadherin signaling

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“…28 Study has found that MTA3 can regulate malignant progression of human cancer through various signaling pathways. 29 -31 Here, we reported that DDX5 knockdown inhibited migration and invasion of BCC cells. However, we will further investigate the expression of DDX5 in the more aggressive BCC subtypes based on their morphologies in our future work.…”

Section: Discussionmentioning

confidence: 89%

DDX5 Silencing Suppresses the Migration of Basal cell Carcinoma Cells by Downregulating JAK2/STAT3 Pathway

Quan

Zhang

Yin

et al. 2019

Technol Cancer Res Treat

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Basal cell carcinoma is driven by the aberrant activation of hedgehog signaling. DEAD (Asp-Glu-Ala-Asp) box protein 5 is frequently overexpressed in human cancer cells and associated with the tumor growth and invasion. The purpose of this study was to investigate the role of DEAD (Asp-Glu-Ala-Asp) box protein 5 in the growth, migration, and invasion of basal cell carcinoma. The role of DEAD (Asp-Glu-Ala-Asp) box protein 5 was detected by quantitative real-time polymerase chain reaction, Western blot, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assay in basal cell carcinoma cells. The associations between JAK2/STAT3 pathway and DEAD (Asp-Glu-Ala-Asp) box protein 5 were analyzed in basal cell carcinoma cells. Results showed that DEAD (Asp-Glu-Ala-Asp) box protein 5 is overexpressed in basal cell carcinoma cells. DEAD (Asp-Glu-Ala-Asp) box protein 5 knockdown inhibited the migration and invasion of basal cell carcinoma cells. DEAD (Asp-Glu-Ala-Asp) box protein 5 knockdown increased the apoptosis of basal cell carcinoma cells induced by tunicamycin. Results found that DEAD (Asp-Glu-Ala-Asp) box protein 5 knockdown increased JAK2 and STAT3 expression in basal cell carcinoma cells. JAK2 inhibitor decreased STAT3 expression and abolished the inhibitory effects of DEAD (Asp-Glu-Ala-Asp) box protein 5 silencing on migration and invasion in basal cell carcinoma cells. In conclusion, these results indicate that DEAD (Asp-Glu-Ala-Asp) box protein 5 is a potential target for inhibiting basal cell carcinoma cells growth, migration, and invasion by downregulating JAK2/STAT3 pathway.

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MTA3 regulates malignant progression of colorectal cancer through Wnt signaling pathway

Cited by 15 publications

References 23 publications

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

lncRNA PCAT1 might coordinate ZNF217 to promote CRC adhesion and invasion through regulating MTA2/MTA3/Snai1/E-cadherin signaling

DDX5 Silencing Suppresses the Migration of Basal cell Carcinoma Cells by Downregulating JAK2/STAT3 Pathway

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