Migration of oral squamous cell carcinoma cells are induced by HGF/c-Met signalling via lamellipodia and filopodia formation

Yasui, Hirofumi; Ohnishi, Yozo; Nakajima, Masahiro; Nozaki, Masami

doi:10.3892/or.2017.5587

Cited by 17 publications

(15 citation statements)

References 45 publications

(49 reference statements)

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“…EGFR and MET inhibitors induced changes in actin cytoskeleton organization of oral squamous cell carcinoma cells. Furthermore, MET inhibitor reduced filopodia and lamellipodia formation, thus decreasing migration of these cells . Miekus et al also observed in MET‐deficient cervical carcinoma cells, that F‐actin was located under the cell membrane and did not form regular stress fibres which were present in control cells.…”

Section: Discussionmentioning

confidence: 93%

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Expression level of EGFR and MET receptors regulates invasiveness of melanoma cells

Pietraszek-Gremplewicz

Simiczyjew

Dratkiewicz

et al. 2019

J Cellular Molecular Medi

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Epidermal and hepatocyte growth factors can stimulate invasive abilities of melanoma cells, while treatment with combination of their receptors' (EGFR and MET, respectively) inhibitors reduces viability of these cells, as we have previously shown. Proposed therapy has potential; however, used drugs block more than one goal effectively, what raises the question about the real target of analysed inhibitors. For this reason, we analysed direct involvement of these receptors in the invasion of melanoma cells inducing EGFR and MET up‐ and down‐regulations in examined cells. Results were acquired with assays evaluating cell migration and invasion (scratch wound assay, Transwell filter‐based method and single‐cell tracking). We revealed that cells' motile abilities are increased after EGFR overexpression and decreased following EGFR and MET silencing. This outcome correlates with elevated (EGFR up‐regulation) or reduced (EGFR/MET down‐regulation) number of formed invadopodia, visualized with immunofluorescence, and their rate of proteolytic abilities, evaluated by fluorescent gelatin degradation assay, and gelatin zymography, compared to control cells. Above‐mentioned data indicate that both—EGFR and MET signalling is directly connected with melanoma cells invasion, what establishes these receptors as promising targets for anti‐cancer treatment.

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Section: Discussionmentioning

confidence: 93%

“…Furthermore, MET inhibitor reduced filopodia and lamellipodia formation, thus decreasing migration of these cells. 43 Miekus et al 44 and MMP-9-mediated degradation of E-cadherin. 49 Therefore, we also analysed proteolytic activity of generated variants of melanoma cells.…”

Section: Discussionmentioning

confidence: 99%

Expression level of EGFR and MET receptors regulates invasiveness of melanoma cells

Pietraszek-Gremplewicz

Simiczyjew

Dratkiewicz

et al. 2019

J Cellular Molecular Medi

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“…In OSCC, c-MET has been shown to be upregulated in OSCC tissues, and its expression was associated with tumor stage (31). In addition, downregulating of c-MET could inhibit OSCC cell proliferation and invasion (32). Thus, in our study, we selected c-MET as a direct target of miR-152, and found that overexpression miR-152 significantly inhibited c-MET and the downstream signaling pathway, c-MET expression was upregulated in OSCC tissues, and inversely correlated with miR-152 expression.…”

Section: Discussionmentioning

confidence: 99%

Function of miR‑152 as tumor suppressor in oral squamous cell carcinoma cells by targeting c‑MET

Wang³

et al. 2017

Oncol Rep

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MicroRNA‑152 (miR‑152) has been reported to be involved in tumor development and progression in multiple cancers. However, the expression level, biological function and regulatory mechanisms of miR‑152 in oral squamous cell carcinoma cells (OSCC) remain unclear. The aims of this study were therefore to investigate the role of miR‑152 in OSCC and the relevant mechanism. It was found that miR‑152 was downregulated in OSCC cell lines and tissues, and that decreased miR‑152 was closely associated with lymph node metastasis, and patient survival rate. In vitro restoration of miR‑152 significantly repressed cell proliferation, colony formation, migration and invasion of OSCC cells. Notably, cellular-mesenchymal to epithelial transition factor (c‑MET) and its downstream signaling pathway (PI3K/AKT) was downregulated in OSCC cells by miR‑152 through direct interactions with its 3' untranslated region. Restoring c‑MET expression attenuated miR‑152-induced inhibitory effects in OSCC cells. In vivo study confirmed that restoration of miR‑152 suppressed tumor growth in xenograft nude mice by repressing c‑MET. In summary, the present study highlight miR‑152 as a tumor suppressor in OSCC through direct targeting c‑MET, rendering miR‑152 a promising therapeutic target for oral squamous cell carcinoma.

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“…The HSC-4 and Ca9-22 human OSCC cell line was used as an experimental model in this study. HSC-4 and Ca9-22 cells are negative for cancer stemness (41) and responsive to HGF and c-Met inhibitor SU11274 (23). Thus, the effects of curcumin on HGF-induced EMT and the invasive and migratory potential of HSC-4 and Ca9-22 cells were investigated.…”

Section: Discussionmentioning

confidence: 99%

Curcumin inhibits epithelial‑mesenchymal transition in oral cancer cells via c‑Met blockade

Ohnishi

Sakamoto

et al. 2020

Oncol Lett

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Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer. OSCC cells are highly invasive, a characteristic that involves epithelial-mesenchymal transition (EMT); the conversion of immotile epithelial cells into motile mesenchymal cells. EMT is involved in the progression of various types of cancer by promoting tumour cell scattering and conferring to these cells cancer stem cell (CSC)-like characteristics, such as self-renewal. Hepatocyte growth factor (HGF) signalling plays an important role in EMT induction and, therefore, contributes to cell invasion and metastasis in cancer. Due to its potential chemopreventative and anti-tumour activities, curcumin has attracted much interest and has been shown to act as a potent EMT inhibitor in various types of cancer. However, at present, the potential effects of curcumin on HGF-induced EMT in OSCC have not been investigated. Here, we demonstrated that HGF signalling could induce EMT in the HSC4 and Ca9-22 OSCC cell lines via the HGF receptor c-Met and downstream activation of the pro-survival ERK pathway. Notably, curcumin inhibited HGF-induced EMT and cell motility in HSC-4 and Ca9-22 cells via c-Met blockade. Therefore, these findings establish curcumin as a candidate drug for OSCC treatment. Furthermore, curcumin was able to effectively inhibit the HGF-induced increase in the levels of vimentin by downregulating the expression of phosphorylated c-Met, an ERK. In conclusion, the results of the present study demonstrated that curcumin was able to reverse HGF-induced EMT, possibly by inhibiting c-Met expression in oral cancer cells, providing a strong basis for the development of novel approaches for the treatment of oral cancer.

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Migration of oral squamous cell carcinoma cells are induced by HGF/c-Met signalling via lamellipodia and filopodia formation

Cited by 17 publications

References 45 publications

Expression level of EGFR and MET receptors regulates invasiveness of melanoma cells

Expression level of EGFR and MET receptors regulates invasiveness of melanoma cells

Function of miR‑152 as tumor suppressor in oral squamous cell carcinoma cells by targeting c‑MET

Curcumin inhibits epithelial‑mesenchymal transition in oral cancer cells via c‑Met blockade

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