Glycoprotein nonmetastatic melanoma protein B accelerates tumorigenesis of cervical cancer in vitro by regulating the Wnt/β-catenin pathway

Xu, Shen; Fan, Yingying; Li, Dongping; Liu, Yan; Xu, Chen

doi:10.1590/1414-431x20187567

Cited by 5 publications

(4 citation statements)

References 34 publications

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“…Additionally, MuSK is also involved in the noncanonical Wnt signaling pathway . Recent publications, however, showed that GPNMB is involved in Wnt/β‐catenin signaling in glioma, cervical cancer, and breast cancer models . These findings bring us one possibility that the KLD of GPNMB is somehow involved in the Wnt signaling pathway and our initial experiments suggested that GPNMB KLD might have some function to support Wnt/β‐catenin signaling (Figure E,F).…”

Section: Discussionmentioning

confidence: 75%

“…36 Recent publications, however, showed that GPNMB is involved in Wnt/β-catenin signaling in glioma, cervical cancer, and breast cancer models. [37][38][39] These findings bring us one possibility that the KLD of GPNMB is somehow involved in the Wnt signaling pathway and our initial experiments suggested that GPNMB KLD might have some function to support Wnt/β-catenin signaling ( Figure 5E,F). Further studies are needed to reveal the mechanism by which the KLD contributes to the tumorigenic function of GPNMB, and identification of the binding partner through this region is essential.…”

Section: Discussionmentioning

confidence: 81%

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Role of the kringle‐like domain in glycoprotein NMB for its tumorigenic potential

et al. 2019

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Glycoprotein NMB (GPNMB) is highly expressed in many types of malignant tumors and thought to be a poor prognostic factor in those cancers, including breast cancer. Glycoprotein NMB is a type IA transmembrane protein that has a long extracellular domain (ECD) and a short intracellular domain (ICD). In general, the ECD of a protein is involved in protein‐protein or protein‐carbohydrate interactions, whereas the ICD is important for intracellular signaling. We previously reported that GPNMB contributes to the initiation and malignant progression of breast cancer through the hemi‐immunoreceptor tyrosine‐based activation motif (hemITAM) in its ICD. Furthermore, we showed that the tyrosine residue in hemITAM is involved in induction of the stem‐like properties of breast cancer cells. However, the contribution of the ECD to its tumorigenic function has yet to be fully elucidated. In this study, we focused on the region, the so‐called kringle‐like domain (KLD), that is conserved among species, and made a deletion mutant, GPNMB(ΔKLD). Enhanced expression of WT GPNMB induced sphere and tumor formation in breast epithelial cells; in contrast, GPNMB(ΔKLD) lacked these activities without affecting its molecular properties, such as subcellular localization, Src‐induced tyrosine phosphorylation at least in overexpression experiments, and homo‐oligomerization. Additionally, GPNMB(ΔKLD) lost its cell migration promoting activity, even though it reduced E‐cadherin expression. Although the interaction partner binding to KLD has not yet been identified, we found that the KLD of GPNMB plays an important role in its tumorigenic potential.

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 81%

Role of the kringle‐like domain in glycoprotein NMB for its tumorigenic potential

et al. 2019

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“…As a classical signaling pathway, the activation of Wnt/ b-catenin signaling pathway is confirmed to be associated with the biological behavior of cancers, such as liver cancer, 28 pancreatic cancer, 29 and CC. 30 Here, the authors investigated whether Wnt/b-catenin signaling pathway engages in the SNHG7-regulated CC occurrence. In this work, it was revealed that the expression of Wnt/b-catenin signaling pathway-related proteins (bcatenin, c-myc, and cyclin D1) was suppressed, whereas that of dickkopf-1 (DKK1, the inhibitor of Wnt/b-catenin signaling pathway) was enhanced by SNHG7 depletion in CC cells.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA SNHG7 Activates Wnt/β-Catenin Signaling Pathway in Cervical Cancer Cells by Epigenetically Silencing DKK1

Chi

Hou

et al. 2020

Cancer Biotherapy and Radiopharmaceuticals

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Background: Cervical cancer (CC) ranks fourth in cancers that resulted in death among women, accumulating the attention of researchers. It has been ascertained that long noncoding RNAs (lncRNAs) are crucial players in the pathological processes of a host of cancers. And, SNHG7 has been reported to enhance the occurrence of various cancers; however, its function in CC sustains obscure. Aim of the Study: This study explored the function of SNHG7 in CC and further investigates the specific molecular mechanism of SNHG7 in regulating CC. Methods: The levels of SNHG7 in CC cells were reflected by quantitative real-time polymerase chain reaction. The functions of SNHG7 on CC tumorigenesis were explored by colony formation, CCK-8 (Cell Counting Kit-8), EdU (ethynyl deoxyuridine), and Western blot assays. The influences of SNHG7 depletion on the binding of EZH2 to DKK1 promoter and H3K27me3 occupancy in DKK1 promoter were studied by chromatin immunoprecipitation assay. Results: SNHG7 was conspicuously higher expressed in CC cells. Knockdown of SNHG7 was detected to ameliorate the malignant behaviors of CC cells. Importantly, the contribution of SNHG7 to CC development was relied on activated Wnt pathway through DDK1-mediated manner. Furthermore, it was confirmed that SNHG7 silencing weakened the binding of EZH2 to DKK1 promoter as well as the occupancy of H3K27me3 in DKK1 promoter. Conclusions: SNHG7 epigenetically silences DKK1 to exacerbate the malignancy of CC via Wnt/b-catenin signaling pathway.

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“…Gefitinib suppresses EMT via the Wnt/β-catenin signaling pathway in CC cells. The Wnt/β-catenin signaling pathway is a major contributor to CC tumorigenesis (17). GSK3β is a known negative regulator of β-catenin.…”

Section: Gefitinib Induces Apoptosis In CC Cellsmentioning

confidence: 99%

Gefitinib suppresses cervical cancer progression by inhibiting cell cycle progression and epithelial‑mesenchymal transition

Zheng

Yang

et al. 2019

Exp Ther Med

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Cervical cancer (CC) is the second most common malignant cancer among women. Gefitinib was one of the first-generation epidermal growth factor receptor-tyrosine kinase inhibitors in clinical trials. However, the underlying mechanism of gefitinib in regulating CC progression remains unknown. In the current study, two CC cell lines, HeLa and Siha, were used to investigate the effects of gefitinib. Cell counting kit-8 assays demonstrated that treatment with gefitinib exerted strong cytotoxicity in HeLa and Siha cells. Flow cytometry was used to examine cell cycle progression and apoptosis. Treatment with gefitinib enhanced the number of cells in the G 0 /G 1 phase and increased apoptosis in HeLa and Siha cells. Furthermore, treatment with gefitinib decreased the protein expression level of Bcl-2 and increased the protein expression level of Bax. Taken together, these results suggest that gefitinib may suppress CC cell proliferation and induce cell cycle arrest and apoptosis. The current study also demonstrated that treatment with gefitinib suppressed epithelial-mesenchymal transition (EMT) as the expression level of the epithelial marker, E-cadherin was increased, while the expression level of the mesenchymal marker, vimentin was decreased. The current study demonstrated that treatment with gefitinib decreased the protein expression levels of phosphorylated-GSK3β and β-catenin, which suggests that gefitinib may be a potential novel therapeutic strategy in CC by suppressing the Wnt/β-catenin signaling pathway and EMT to inhibit tumor metastasis in CC cells. In conclusion, gefitinib may suppress the EMT process during cell invasion and induce cell apoptosis and cell cycle arrest via inhibition of the Wnt/β-catenin signaling pathway.

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Glycoprotein nonmetastatic melanoma protein B accelerates tumorigenesis of cervical cancer in vitro by regulating the Wnt/β-catenin pathway

Cited by 5 publications

References 34 publications

Role of the kringle‐like domain in glycoprotein NMB for its tumorigenic potential

Role of the kringle‐like domain in glycoprotein NMB for its tumorigenic potential

Long Noncoding RNA SNHG7 Activates Wnt/β-Catenin Signaling Pathway in Cervical Cancer Cells by Epigenetically Silencing DKK1

Gefitinib suppresses cervical cancer progression by inhibiting cell cycle progression and epithelial‑mesenchymal transition

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