Differential Expression of <i>ADAM23, CDKN2A (P16), MMP14 </i>and<i> VIM </i>Associated with Giant Cell Tumor of Bone

Conceição, André Luis Giacometti; Babeto, Erica; Cândido, Natália Maria; Franco, Fernanda Craveiro; Zuccari, Débora Aparecida Pires de Campos; Bonilha, Jane Lopes; Cordeiro, José Antônio; Calmon, Marília Freitas; Rahal, Paula

doi:10.7150/jca.11238

Cited by 8 publications

(5 citation statements)

References 86 publications

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“… 17 Additionally, several researches stated that VIM expression was downregulated in well‐differentiated endometrial cancer cells and giant cell tumor of bone. 18 , 19 Overexpression of VIM promotes migration, invasion, and metastasis of CRC cells. 20 To our knowledge, miRNA play its biological function by suppressing target gene expression.…”

Section: Discussionmentioning

confidence: 99%

“…Battaglia et al have proved that VIM intermediate filaments are essential for the plasticity of mesenchymal cells under normal physiological conditions and cancer cell migration during epithelial–mesenchymal transition 17 . Additionally, several researches stated that VIM expression was downregulated in well‐differentiated endometrial cancer cells and giant cell tumor of bone 18,19 . Overexpression of VIM promotes migration, invasion, and metastasis of CRC cells 20 .…”

Section: Discussionmentioning

confidence: 99%

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MiR‐630 suppresses non‐small cell lung cancer by targeting vimentin

Wang

et al. 2022

Clinical Laboratory Analysis

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Objective This study aimed to clarify the function of miR‐630 on non‐small cell lung cancer (NSCLC) cells. Methods Quantitative real‐time PCR was utilized to detect the mRNA expression of miR‐630 and vimentin (VIM) in NSCLC tissues and cells. The protein expression of VIM, P53, Caspase‐3, Bcl‐2, Bax and JAK2/STAT3 was evaluated via Western blot. Dual‐luciferase reporter assay was applied to evaluate whether VIM is the target gene of miR‐630. The migration, invasion, proliferation and apoptosis of NSCLC cells were examined by wound‐healing assay, transwell assay, CCK‐8 assay, and flow cytometry, respectively. Results MiR‐630 was lowly expressed in NSCLC tissues and cells, while VIM was highly expressed in NSCLC cells. Dual‐luciferase reporter assay data validated that miR‐630 directly targeted VIM. MiR‐630 overexpression inhibited VIM expression, but the inhibition of miR‐630 upregulated VIM expression. Besides, miR‐630 mimics restrained cell migration, invasion, and proliferation, and promoted NSCLC cell apoptosis. Whereas, VIM overexpression partly attenuated the inhibitory effect of miR‐630 on NSCLC cells. Moreover, miR‐630 mimics impeded p‐JAK2 and p‐STAT3 protein expression; and miR‐630 inhibitor upregulated p‐STAT3 and VIM protein expression, which was reversed after the addition of STAT3 inhibitor C188‐9. Conclusion MiR‐630 constrained the progression of NSCLC by inhibiting JAK2/STAT3 pathway and downregulating VIM expression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MiR‐630 suppresses non‐small cell lung cancer by targeting vimentin

Wang

et al. 2022

Clinical Laboratory Analysis

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“…They showed that high expression of MAP2K3 was significantly correlated with CA125 level (p < 0.001), tumor size (p = 0.001), lymph node metastasis (p = 0.008), depth of myometrial invasion (p < 0.001), and FIGO stage (p < 0.001), indicating MKK3 as a poor prognostic biomarker [54]. Conceicao et al, conducted immunohistochemical staining on 24 samples of giant cell tumors of bone and normal tissues and reported higher expression of the MKK3, MMP14, TIMP2, and VIM genes in tumor than the normal counterpart, suggesting their involvement in invasion and metastasis [55]. With the tissue microarray (TMA) performed in a cohort of 189 colorectal cancer patients, our study identified MKK3 as a poor prognostic marker, correlating significantly high MKK3 staining with short overall survival (OS) in late-stage CRC patients [1].…”

Section: Discussionmentioning

confidence: 99%

Dissection of the MKK3 Functions in Human Cancer: A Double-Edged Sword?

Piastra¹,

Pranteda²,

Bossi³

2022

Cancers

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The role played by MKK3 in human cancer is controversial. MKK3 is an evolutionarily conserved protein kinase that activates in response to a variety of stimuli. Phosphorylates, specifically the p38MAPK family proteins, contribute to the regulation of a plethora of cellular processes such as proliferation, differentiation, apoptosis, invasion, and cell migration. Genes in carcinogenesis are classified as oncogenes and tumor suppressors; however, a clear distinction is not always easily made as it depends on the cell context and tissue specificity. The aim of this study is the examination of the potential contribution of MKK3 in cancer through a systematic analysis of the recent literature. The overall results reveal a complex scenario of MKK3’s involvement in cancer. The oncogenic functions of MKK3 were univocally documented in several solid tumors, such as colorectal, prostate cancer, and melanoma, while its tumor-suppressing functions were described in glioblastoma and gastric cancer. Furthermore, a dual role of MKK3 as an oncogene as well as tumor a suppressor has been described in breast, cervical, ovarian, liver, esophageal, and lung cancer. However, overall, more evidence points to its role as an oncogene in these diseases. This review indicates that the oncogenic and tumor-suppressing roles of MKK3 are strictly dependent on the tumor type and further suggests that MKK3 could represent an efficient putative molecular target that requires contextualization within a specific tumor type in order to adequately evaluate its potential effectiveness in designing novel anticancer therapies.

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“…The CDKN2A gene also known as p16INK4 is thought to help suppress tumors (Foulkes et al 1997). The CDKN2A protein is critical for inhibiting cell cycle progression, and the down-regulation of p16 could lead to increased cell proliferation and may contribute to the pathogenesis of several cancers (Conceição et al 2015). In a study by Chen Z et al, they analyzed CDKN2A levels in 33 tumors and found that CDKN2A may be a promising prognostic biomarker with potential molecular mechanisms to in uence the survival outcomes of cancer patients (Chen et…”

Section: Molecular Dockingmentioning

confidence: 99%

Exploring the hub genes and mechanisms of Daphne altaica treating esophageal squamous cell carcinoma based on network pharmacology and bioinformatics analysis

Hailati

Talihati

Abudurousuli

et al. 2023

J Cancer Res Clin Oncol

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Esophageal squamous cell carcinoma (ESCC), is a frequent digestive tract malignant carcinoma with a high fatality rate. Daphne altaica. (D. altaica), a medicinal plant that is frequently employed in Kazakh traditional medicine, and which has traditionally been used to cure cancer and respiratory conditions, but research on the mechanism is lacking. Therefore, we examined and veri ed the hub genes and mechanism of D. altaica treating ESCC. MethodsActive compounds and targets of D. altaica were screened by databases such as TCMSP, and ESCC targets were screened by databases such as GeneCards and constructed the compound-target network and PPI network. Meantime, datasets between tissues and adjacent non-cancerous tissues from GEO database (GSE100942, GPL570) were analyzed to obtain DEGs using the limma package in R. Hub genes were validated using data from the Kaplan-Meier plotter database, TIMER2.0 and GEPIA2 databases.Finally, AutoDock software was used to predict the binding sites through molecular docking. ResultsIn total, 830 compound targets were obtained from TCMSP and other databases. And 17710 disease targets were acquired based on GeneCards and other databases. And we constructed the compoundtarget network and PPI network. Then, 127 DEGs were observed (82 up-regulated and 45 down-regulated genes). Hub genes were screened including TOP2A, NUF2, CDKN2A, BCHE, and NEK2, and had been validated with the help of several publicly available databases. Finally, molecular docking results showed more stable binding between ve hub genes and active compounds . ConclusionsIn the present study, ve hub genes were screened and validated, and potential mechanisms of action were predicted, which could provide a theoretical understanding of the treatment of ESCC with D. altaica.2. In the above screening outcomes, we got the two most active compounds of the drug (Apigenin and Luteolin). Using the TCMSP and PubChem databases, we obtained the protein structures of the compounds (Kim et al. 2019). In the same process as in the previous step, the protein was modi ed in AutoDock4.2.6 to remove the water and add hydrogen, and the ligand les were saved in PDBQT format.3. To perform molecular docking, we imported the above two structure les into AutoDock4.2.6. The minimum binding energy was calculated using the PDBQT format. The PDBQT format was then converted to the PDB format using the OpenBabel software (O'Boyle et al. 2011). 4. Finally, PyMOL2.5 software was used to visualize the molecular docking maps.

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Differential Expression of ADAM23, CDKN2A (P16), MMP14 and VIM Associated with Giant Cell Tumor of Bone

Cited by 8 publications

References 86 publications

MiR‐630 suppresses non‐small cell lung cancer by targeting vimentin

MiR‐630 suppresses non‐small cell lung cancer by targeting vimentin

Dissection of the MKK3 Functions in Human Cancer: A Double-Edged Sword?

Exploring the hub genes and mechanisms of Daphne altaica treating esophageal squamous cell carcinoma based on network pharmacology and bioinformatics analysis

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