Imatinib-associated matrix metalloproteinase suppression in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in vitro

Umbreit, Claudia; Aderhold, Christoph; Faber, Anne; Sauter, Alexander; Hofheinz, Ralf–Dieter; Stern‐Straeter, Jens; Hoermann, Karl; Schultz, Johannes

doi:10.3892/or.2014.3225

Cited by 12 publications

(8 citation statements)

References 51 publications

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“…Besides that, it has been found that the activation of Wnt/β-catenin pathway can promote the progression of human cancers [ 15 ]. β-catenin belonging to the Wnt/β-catenin signaling pathway was reported to participate in tumorigenesis [ 16 ]. Wnt/β-catenin signaling pathways was also identified as therapeutic targets in cancer [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-638 inhibits the progression of breast cancer through targeting HOXA9 and suppressing Wnt/β-cadherin pathway

Zhang

Dong

et al. 2021

World J Surg Onc

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Background Previous studies had shown that microRNA-638 (miR-638) exhibited different effects in malignant tumors. Moreover, the function of miR-638 has not been reported in breast cancer. Hence, we designed this research to explore the function of miR-638 in breast cancer. Methods Firstly, miR-638 expressions were measured in breast cancer tissues via RT-qPCR. Protein expressions were detected through immunocytochemical (IHC) assay and western blot analysis. Then, Cell Counting Kit-8 (CCK-8) assay and Transwell assay were conducted to observe proliferation and motility of the cells. Dual luciferase assay was performed to confirm the binding site between miR-638 and Homeobox protein Hox-A9 (HOXA9). Results Reduced expression of miR-638 was detected in breast cancer. And low miR-638 expression was related to poor prognosis in patients with breast cancer. Functionally, the viability, migration, and invasion of the breast cancer cells were suppressed by miR-638 overexpression. Furthermore, miR-638 can directly bind to HOXA9, and increased expression of HOXA9 was also detected in breast cancer. In particular, HOXA9 upregulation can impair anti-tumor effect of miR-638 in breast cancer, and miR-638 can hinder the Wnt/β-cadherin pathway and epithelial-mesenchymal transition (EMT) in breast cancer. Conclusion miR-638 inhibits breast cancer progression through binding to HOXA9.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-638 inhibits the progression of breast cancer through targeting HOXA9 and suppressing Wnt/β-cadherin pathway

Zhang

Dong

et al. 2021

World J Surg Onc

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“…The role of c-kit during EMT remains unclear. Also known as cluster of differentiation (CD)117, c-kit is a member of the receptor tyrosine kinase family, and acts as oncogene in several tumours ( 19 ). Tang et al ( 20 ) have previously described an important function for c-kit in the progression of salivary adenoid cystic cancer by orchestrating EMT.…”

Section: Introductionmentioning

confidence: 99%

Lapatinib-induced mesenchymal-epithelial transition in squamous cell carcinoma cells correlates with unexpected alteration of β-catenin expression

et al. 2016

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The epithelial-mesenchymal transition (EMT) is a key developmental program that is often activated during cancer progression, and may promote resistance of cancer cells to therapy. Inhibiting EMT appears to be crucial to inhibit drug resistance. The mesenchymal-epithelial transition (MET), which is the reverse program of EMT in metastases, is characterized by the upregulation of epithelial adhesive proteins such as E-cadherin, and downregulation of mesenchymal proteins such as vimentin. The sensitivity of cancer cells to epithelial growth factor receptor (EGFR) inhibitor may be increased by inducing MET in these cells. Therefore, it is of clinical importance to specify the phenotype of cancer cells in order to overcome the phenomenon of drug resistance. The aim of the present study was to investigate the expression pattern of specific markers in squamous cell carcinoma (SCC) cells following stimulation with lapatinib and gefitinib. For this purpose, the head and neck (HN) SCC cell lines HNSCC22B and HNSCC11A were incubated with 0.5 and 2 µg/ml lapatinib and gefitinib, and the levels of E-cadherin, vimentin, matrix metalloproteinase-14, c-kit and β-catenin were detected by immunocytochemistry and enzyme-linked immunosorbent assay at 5, 24 and 96 h post-incubation. The results indicated that, compared with HNSCC22B cells, the protein expression levels of vimentin increased, whereas those of E-cadherin reduced, in non-stimulated HNSCC11A cells. In addition, the protein expression levels of β-catenin were altered in the epithelial- and mesenchymal-associated SCC cell lines following treatment with lapatinib and gefitinib. Furthermore, lapatinib induced the downregulation of vimentin and upregulation of E-cadherin in HNSCC11A cells in a time-dependent manner. This suggests that the sensitivity of cancer cells to lapatinib may be improved by inducing MET in these cells. In summary, the results of the present study demonstrated that lapatinib-induced MET led to an unexpected alteration of the protein expression levels of β-catenin in SCC cells. Further studies on the mechanistic role of MET are required in order to increase the sensitivity of cancer cells to EGFR inhibitor and block the EMT process in these cells.

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“…36,37 MMPs are capable of ECM remodeling, favoring the invasion and proliferation of tumor cells. 38,39 MMPs have been detected in both cyst fluids and wall tissue extracts of various odontogenic cysts and odontogenic tumors, including ABs, suggesting that these enzymes play a key role in regulation of tumor and cyst growth. [40][41][42][43] In the present research, the expression of MMP in AB and its effect on tumor cell invasion and the prognosis of patients were varied.…”

Section: Discussionmentioning

confidence: 99%

Expression of Matrix Metalloproteinases in Ameloblastomas and Ameloblastic Carcinoma: Systematic Review and Meta-analysis

Yongmei¹,

Zhong²,

Ye³

et al. 2019

Exploratory Research and Hypothesis in Medicine

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Objective: This study aimed to examine the difference in expression of matrix metalloproteinases (MMPs) in ameloblastoma and other benign tumors or normal tissue of the jaw, and ameloblastic carcinoma, and to investigate the correlation of expression of MMPs with patient prognosis. Methods: Studies were identified in the major electronic databases (Medline, EMBASE and Cochrane Library) using the keywords "matrix metalloproteinases" and "ameloblastoma" OR "ameloblastic carcinoma", and a quantitative meta-analysis was conducted. Results: Fourteen studies were included in this systematic review. Twelve studies representing a total number of 471 cases qualified for the meta-analysis. The analysis revealed a higher MMP-2 expression in ameloblastoma than in the other benign odontogenic tumors, showing a significant inter-group difference (odds ratio [OR]: 5.33; 95% confidence interval (CI): [1.36, 25.62]; p = 0.02). A lower MMP-2 expression was found for the ameloblastoma than in the ameloblastic carcinoma, with a non-significant inter-group difference (OR: 0.12; 95% CI: [0.01, 1.02]; p = 0.05). Finally, a lower MMP-9 expression was found for the follicular subgroup compared to that in other subgroups of ameloblastoma, showing a significant inter-group difference (OR: 0.15; 95% CI: [0.05, 0.48]; p = 0.001). Conclusions: We found that MMP-2 expression in ameloblastoma is higher than that in other benign tumors or normal tissue of jaw, and that MMP-9 expression in the follicular subgroup of ameloblastoma is lower than that in other pathology subgroups of ameloblastoma. What is more important, the MMPs expression in ameloblastoma was found to be significantly correlated with many clinicopathologic features of ameloblastoma. However, some limitations weakened the power of this meta-analysis.

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Imatinib-associated matrix metalloproteinase suppression in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in vitro

Cited by 12 publications

References 51 publications

MicroRNA-638 inhibits the progression of breast cancer through targeting HOXA9 and suppressing Wnt/β-cadherin pathway

MicroRNA-638 inhibits the progression of breast cancer through targeting HOXA9 and suppressing Wnt/β-cadherin pathway

Lapatinib-induced mesenchymal-epithelial transition in squamous cell carcinoma cells correlates with unexpected alteration of β-catenin expression

Expression of Matrix Metalloproteinases in Ameloblastomas and Ameloblastic Carcinoma: Systematic Review and Meta-analysis

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