RETRACTED ARTICLE: Downregulation of nicotinamide N-methyltransferase inhibits migration and epithelial-mesenchymal transition of esophageal squamous cell carcinoma via Wnt/β-catenin pathway

Cui, Yanyan; Zhang, Luyu; Wang, Wenjie; Ma, Shanshan; Liu, Hongtao; Zang, Xingxing; Zhang, Yanting; Guan, Fangxia

doi:10.1007/s11010-019-03573-0

Cited by 32 publications

(38 citation statements)

References 24 publications

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“…EMT is a complex process. It has been proved that Wnt/β-catenin signaling pathway is activated during EMT, while Wnt/β-catenin pathway inactivation can inhibit and reverse EMT [33,34]. Currently, the mRNA and protein levels of E-cadherin, N-cadherin, Vimentin, and MMP9 in the ESCC cells incubated with T-96 are studied.…”

Section: Discussionmentioning

confidence: 99%

Demethylzelasteral inhibits proliferation and EMT via repressing Wnt/β-catenin signaling in esophageal squamous cell carcinoma

Yu¹,

Wang²,

Liu³

et al. 2021

J. Cancer

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As a kind of tumor commonly seen, no effective treatment is available for esophageal squamous cell carcinoma (ESCC). Therefore, seeking a new treatment is urgent. Demethylzeylasteral (T-96) isolated from Tripterygium wilfordii root bark embraces outstanding good antitumor activity. However, as for the mechanism of T-96 work on ESCC cells, it is rarely reported. In this study, we found that T-96 has inhibition when ESCC cells are proliferating, migrating and cloning. Moreover, relevant effects are influenced by dose and time. And T-96 can result in the stop of G2/M phase and induce apoptosis of ESCC cells. In addition, the expressions of Cyclin B1, Cyclin D1, Bcl-2, PARP1 and Survivin were decreased after starch demethylation. Despite of this, Bax and PARP1's expressions went up. To add up, there was an obvious increase in the expression of E-cadherin, while that of N-cadherin, Vimentin and MMP9 decreased after T-96 treatment. Moreover, the expression of Wnt/β-Catenin pathway, which concerns proteins β-Catenin, c-Myc and Wnt3a decreased. Our study shows that T-96 inhibits the proliferation and migration of esophageal cancer cells through Wnt/β-catenin pathway. Moreover, it gives rise to cell cycle arrest and apoptosis. According to the research results, T-96 tends to be put into use when treating ESCC patients, thus laying the experimental foundation for clinical research.

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Section: Discussionmentioning

confidence: 99%

Demethylzelasteral inhibits proliferation and EMT via repressing Wnt/β-catenin signaling in esophageal squamous cell carcinoma

Yu¹,

Wang²,

Liu³

et al. 2021

J. Cancer

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“…An association between the elevated expression of NNMT and several cancers, including pancreatic and colorectal cancers, has been reported [ 15 , 16 , 17 , 18 , 19 ], and the potential of NNMT as a blood tumor marker for bladder and colorectal cancer has been suggested [ 17 , 20 ]. Furthermore, evidence was also provided that there is a correlation between the downregulation of NNMT in cells and lower rates of cell migration [ 15 ]. NNMT expression is upregulated in pancreatic cancer, where levels of the NNMT enzyme correlate with an increased risk of death.…”

Section: Discussionmentioning

confidence: 99%

Scale-Up Evaluation of a Composite Tumor Marker Assay for the Early Detection of Renal Cell Carcinoma

et al. 2020

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The early detection of renal cell carcinoma (RCC) using tumor markers remains an attractive prospect for the potential to downstage the disease. To validate the scale-up clinical performance of potential tumor markers for RCC (as a single marker and as a composite tumor marker composed of nicotinamide N-methyltransferase (NNMT), L-Plastin (LCP1), and non-metastatic cells 1 protein (NM23A)), the scale-up assay was performed. Patients with RCC from multiple domestic institutes were included in the clinical evaluation for reassessment and improvement of the established triple markers of our product. For the diagnostic performance of the composite markers, the best-split cutoff points of each marker (147 pg/mL for NNMT, 1780 pg/mL for LCP1, and 520 pg/mL for NM23A) were installed. Serum levels of NNMT, LCP1, and NM23A were greatly increased in subjects with RCC (p < 0.0001). In 1042 blind sample tests with control individuals (n = 500) and patients with RCC (n = 542), the diagnostic sensitivity and specificity of the composite three-marker assay were 0.871 and 0.894, respectively, and the resulting AUC (Area under Curve) of ROC (Receiver Operating Characteristic) was 0.917. As a single marker, the diagnostic accuracies of NNMT, LCP1, and NM23A, as estimated by ROC, were 0.833, 0.844, and 0.601, respectively. The composite three-marker assay with NNMT, LCP1, and NM23A is a more improved novel serum marker assay for the early detection of RCC in cases of renal mass or unknown condition. The NNMT, LCP1, and NM23A triple marker assay could be a powerful diagnostic tumor marker assay to screen the early stage of RCC.

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“…The epithelial‐mesenchymal transition (EMT) process has become an important mechanism for the distant metastasis of epithelial malignant tumors, including ESCC 11 . EMT is usually characterized by downregulation of epithelial molecules (E‐cadherin) and upregulation of mesenchymal markers (N‐cadherin, vimentin).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of SIX4 indicates poor clinical outcome and promotes tumor growth and cell metastasis in esophageal squamous cell carcinoma

Jiang²,

Yan

et al. 2021

Thoracic Cancer

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Background The role of sine oculis homeobox 4 (SIX4) has been found in some malignant tumors. However, there have been few studies on the function of SIX4 in esophageal squamous cell carcinoma (ESCC). This study aimed to explore the regulatory mechanism of SIX4 in ESCC. Methods RT‐qPCR and Western blot analysis were used to measure mRNA and protein expression. The function of SIX4 was investigated using CCK‐8, colony formation, flow cytometry, wound healing and transwell assays. A mouse xenograft tumor assay was designed to perform in vivo experiments. Results SIX4 was upregulated in ESCC and indicated poor clinical outcomes in ESCC patients. Functionally, knockdown of SIX4 inhibited cell proliferation and induced apoptosis in ESCC. In addition, the silencing of SIX4 inhibited cell migration, invasion and EMT in ESCC. More importantly, upregulation of SIX4 could activate the PI3K/AKT pathway in ESCC cells and promote tumor growth in vivo. Conclusions Upregulation of SIX4 indicates poor clinical outcomes in ESCC patients and promotes tumor growth and cell metastasis in ESCC.

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RETRACTED ARTICLE: Downregulation of nicotinamide N-methyltransferase inhibits migration and epithelial-mesenchymal transition of esophageal squamous cell carcinoma via Wnt/β-catenin pathway

Cited by 32 publications

References 24 publications

Demethylzelasteral inhibits proliferation and EMT via repressing Wnt/β-catenin signaling in esophageal squamous cell carcinoma

Demethylzelasteral inhibits proliferation and EMT via repressing Wnt/β-catenin signaling in esophageal squamous cell carcinoma

Scale-Up Evaluation of a Composite Tumor Marker Assay for the Early Detection of Renal Cell Carcinoma

Upregulation of SIX4 indicates poor clinical outcome and promotes tumor growth and cell metastasis in esophageal squamous cell carcinoma

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