N-cadherin in cancer metastasis, its emerging role in haematological malignancies and potential as a therapeutic target in cancer

Mrozik, Krzysztof M.; Blaschuk, Orest W.; Cheong, Chee Man; Zannettino, Andrew C.W.; Vandyke, Kate

doi:10.1186/s12885-018-4845-0

Cited by 274 publications

(225 citation statements)

References 195 publications

(220 reference statements)

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“…PCNA is an important replication accessory factor that supports DNA replication, repair and recombination, and cell cycle regulation [34,35]. Abnormal expression of the N-cadherin is a crucial biomarker of epithelial-to-mesenchymal transition in many cancer types, promoting the aggressiveness of tumors [36]. As one of the most studied MMPs, MMP-9 is well-known for the key roles in invasion of cancer cells and metastasis of tumors [37].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA NCK1-AS1 promotes the tumorigenesis of glioma through sponging microRNA-138-2-3p and activating the TRIM24/Wnt/β-catenin axis

Huang

et al. 2020

J Exp Clin Cancer Res

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Background: Glioma is a common brain malignancy with high mortality. The competing endogenous RNA (ceRNA) networks may play key roles in cancer progression. This study was conducted to probe the role of long noncoding RNA (lncRNA) NCK1-AS1 in glioma progression and the involved mechanisms.Methods: Microarray analyses were performed to explore the lncRNAs/miRNAs/genes with differential expression in glioma. NCK1-AS1 levels in glioma tissues and normal brain tissues, and in glioma cell lines and normal human glial cells were identified. The interactions among NCK1-AS1, miR-138-2-3p and TRIM24 were validated through luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. Gain-and loss-of functions of NCK1-AS1, miR-138-2-3p and TRIM24 were performed to identify their roles in the behaviors of glioma cells. The activity of the Wnt/β-catenin pathway was measured. In vivo experiments were performed as well.Results: High expression of NCK1-AS1 was found in glioma tissues and cells, especially in U251 cells. Online predictions and the integrated experiments identified that NCK1-AS1 elevated the TRIM24 expression through sponging miR-138-2-3p, and further activated the Wnt/β-catenin pathway. Artificial silencing of NCK1-AS1 or upregulation of miR-138-2-3p led to inhibited proliferation, invasion and migration but promoted cell apoptosis of U251 cells, while up-regulation of TRIM24 reversed these changes, and it activated the Wnt/β-catenin pathway. The in vitro results were reproduced in in vivo experiments.Conclusions: Our study suggested that NCK1-AS1 might elevate TRIM24 expression and further activate the Wnt/βcatenin pathway via acting as a ceRNA for miR-138-2-3p. Silencing of NCK1-AS1 might inhibit the progression of glioma.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA NCK1-AS1 promotes the tumorigenesis of glioma through sponging microRNA-138-2-3p and activating the TRIM24/Wnt/β-catenin axis

Huang

et al. 2020

J Exp Clin Cancer Res

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“…Immunofluorescence staining confirmed the inhibition of vimentin expression by puerarin ( Figure 3C). We next detected the expression of N-cadherin in subcutaneous xenograft mouse models (26). Compared with the control group, the IHC staining of N-cadherin was significantly lighter in the puerarin group ( Figure 3C).…”

Section: Puerarin Inhibited Hcc Epithelial-mesenchymal Transitionmentioning

confidence: 98%

Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition

Zhou

Xue

Wang

et al. 2020

Braz J Med Biol Res

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Erratum for: "Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition" [Braz J Med Biol Res (2020) 53(4): e8882] Yuan Zhou 0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0The authors would like to correct the Corresponding authors' names and emails and the Acknowledgments section of the article "Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition". The Editors highlight that the information presented in the original version was provided by the authors at submission and revision. In addition, the authors had the opportunity to correct the information during proofreading, before approving for publication.Correspondence: Haozhen Ren: orenhaozhen1984@163.com4 | Jinglin Wangocw20120817@163.com4 *These authors contributed equally to this study.Braz J Med Biol Res | AbstractHepatocellular carcinoma (HCC) is one of the most common primary malignant tumors of the liver worldwide. Liver resection and transplantation are currently the only effective treatments; however, recurrence and metastasis rates are still high. Previous studies have shown that the epithelial-mesenchymal transition (EMT) is a key step in HCC invasion and metastasis. Inhibition of EMT has become a new therapeutic strategy for tumors. Recently, puerarin, a well-characterized component of traditional Chinese medicine, has been isolated from Pueraria radix and exerts positive effects on many diseases, particularly cancers. In this study, CCK-8, EdU immunofluorescence, colony formation, wound healing, and migration assays were used to detect the effects of puerarin on HCC cells. We further analyzed the relationship between puerarin and miR-21/PTEN/EMT markers in HCC cell lines. Our results showed that HCC cell proliferation, migration, invasion, tumor formation, and metastasis were reduced by puerarin in vitro and in vivo. Additionally, puerarin inhibited the EMT process of HCC by affecting the expression of Slug and Snail. Moreover, oncogenic miR-21 was inhibited by puerarin, coupled with an increase in the tumor suppressor gene PTEN. Increasing miR-21 expression or decreasing PTEN expression reversed the inhibition effects of puerarin in HCC. These data confirmed that puerarin affects HCC through the miR-21/PTEN/EMT regulatory axis. Overall, puerarin may represent a chemopreventive and/or chemotherapeutic agent for HCC treatment.

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“…32 Accumulating evidence suggests that EMT is the initiation step of cancer metastasis involving the downregulation of epithelial markers, such as E-cadherin and upregulation of mesenchymal markers, such as N-cadherin. 33,34 Various signaling pathways are involved in the induction of EMT, include TGF-β1, Wnt-β-catenin, Notch, Hedgehog, and tyrosine kinases. 32,35 TGF-β1 is an inflammatory cytokine and a promoter and supporter of EMT.…”

Section: Discussionmentioning

confidence: 99%

<p>Paeonol Inhibits Pancreatic Cancer Cell Migration and Invasion Through the Inhibition of TGF-β1/Smad Signaling and Epithelial-Mesenchymal-Transition</p>

Cheng

Chen

Tang

et al. 2020

CMAR

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These authors contributed equally to this workPurpose: Paeonol, a natural product derived from the root of Cynanchum paniculatum (Bunge) K. Schum and the root of Paeonia suffruticosa Andr. (Ranunculaceae) has attracted extensive attention for its anti-cancer proliferation effect in recent years. The present study examined the role of paeonol in suppressing migration and invasion in pancreatic cancer cells by inhibiting TGF-β1/Smad signaling. Methods: Cell viability was evaluated by MTT and colonial formation assay. Migration and invasion capabilities were examined by cell scratch-wound healing assay and the Boyden chamber invasion assay. Western Blot and qRT-PCR were used to measure the protein and RNA levels of vimentin, E-cadherin, N-cadherin, and TGF-β1/Smad signaling. Results: At non-cytotoxic dose, 100 μΜ and 150 μΜ of paeonol showed significant antimigration and anti-invasion effects on Panc-1 and Capan-1 cells (p<0.01). Paeonol inhibited epithelial-mesenchymal-transition by upregulating E-cadherin, and down regulating N-cadherin and vimentin expressions. Paeonol inhibited TGF-β1/Smad signaling pathway by downregulating TGF-β1, p-Smad2/Smad2 and p-Smad3/Smad3 expressions. Further, TGF-β1 attenuated the anti-migration and anti-invasion capacities of paeonol in Panc-1 and Capan-1 cells. Conclusion: These findings revealed that paeonol could suppress proliferation and inhibit migration and invasion in Panc-1 and Capan-1 cells by inhibiting the TGF-β1/Smad pathway and might be a promising novel anti-pancreatic cancer drug.

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N-cadherin in cancer metastasis, its emerging role in haematological malignancies and potential as a therapeutic target in cancer

Cited by 274 publications

References 195 publications

Long non-coding RNA NCK1-AS1 promotes the tumorigenesis of glioma through sponging microRNA-138-2-3p and activating the TRIM24/Wnt/β-catenin axis

Long non-coding RNA NCK1-AS1 promotes the tumorigenesis of glioma through sponging microRNA-138-2-3p and activating the TRIM24/Wnt/β-catenin axis

Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition

<p>Paeonol Inhibits Pancreatic Cancer Cell Migration and Invasion Through the Inhibition of TGF-β1/Smad Signaling and Epithelial-Mesenchymal-Transition</p>

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