Epithelial-Mesenchymal Transition in Skin Cancers: A Review

Hodorogea, Anastasia; Călinescu, Andreea; Antohe, Mihaela; Balaban, Mihaela; Nedelcu, Roxana Ioana; Turcu, Gabriela; Ion, Daniela Adriana; Bădărău, Ioana Anca; Popescu, C; Popescu, Raluca; Popp, Cristiana; Cioplea, Mirela; Nichita, Luciana; Hulea, Ionela; Brînzea, Alice

doi:10.1155/2019/3851576

Cited by 59 publications

(50 citation statements)

References 109 publications

(130 reference statements)

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“…EMT is involved in the metastatic progression of various malignancies. [20][21][22] We measured the expression of EMTassociated factors to determine the EMT process after knocking-down the expression of CMTM2. As compared to Huh-7-NC cells, the epithelial markers E-cadherin and…”

Section: Down-regulated Cmtm2 Promotes Hcc Metastasis Through Inducinmentioning

confidence: 99%

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Zhang¹,

Tian²,

Bei³

et al. 2020

OTT

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Background: Our recent study identified that human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) was deregulated in hepatocellular carcinoma (HCC) tissues and posed as a potential tumor suppressor. However, the mechanism of CMTM2 in HCC occurrence and development has not been well elaborated. Materials and Methods: The expression of CMTM2 was knocked-down by RNA interruption in Huh-7 and SMMC7721 cells. Cell proliferation ability was detected by CCK8 test and colony formation assay. The cell invasion and migration were measured by wound healing and Transwell assay. Results: We found that the cell proliferation was significantly increased by interruption of CMTM2 expression, both in Huh-7 and SMMC7721 cells. Moreover, down-regulated CMTM2 could promote the invasion and migration ability of HCC cells through inducing the epithelial-mesenchymal transition (EMT) process. We further discovered that both the expression of CMTM2 and the EMT-associated marker E-cadherin were decreased in the same thirty cases of HCC tissues compared with the corresponding adjacent non-tumor tissues. Pearson correlation test showed that there was a significantly positive correlation between CMTM2 and E-cadherin in HCC tissues (P<0.05). Conclusion: Based on the results of cell model and HCC tissues, our study suggests that down-regulated CMTM2 promotes HCC metastasis through inducing the EMT process.

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Section: Down-regulated Cmtm2 Promotes Hcc Metastasis Through Inducinmentioning

confidence: 99%

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Zhang¹,

Tian²,

Bei³

et al. 2020

OTT

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“…Markers of EMT are the increase of Slug [ 15 ] and a decline of E-cadherin [ 16 ] expression. Notably, the presence of HGF promoted Slug expression ( Figure 4 B) and affected the staining of E-cadherin (E-CAD) ( Figure 4 C), but the co-treatment with DPI counteracted these effects.…”

Section: Resultsmentioning

confidence: 99%

The Interplay between HGF/c-met Axis and Nox4 in BRAF Mutated Melanoma

Beretti

Farnetani

Bonetti

et al. 2021

IJMS

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Background: Melanoma is the leading cause of death due to cutaneous malignancy and its incidence is on the rise. Several signaling pathways, including receptor tyrosine kinases, have a role in the development and progression of melanocytic lesions and malignant melanoma. Among those, the hepatocyte growth factor (HGF)/c-met axis is emerging as a critical player because it can play a role in drug resistance. Indeed, 50% of melanoma patients present BRAF mutations, however, all responders develop resistance to the inhibitors typically within one year of treatment. Interestingly, BRAF inhibitors induce reactive oxygen species (ROS) in melanoma cells, therefore, the aim of this study was to investigate a possible interplay between HGF/c-met and ROS sources, such as NADPH oxidases (Nox). Methods: The expression of c-met and Nox were quantified in 60 patients with primary cutaneous melanoma. In vitro experiments on melanoma primary cells and the cell line were performed to dissect the underpinned molecular mechanism. Results: The outcome of interest was the correlation between the high positivity for both Nox4 and c-met and metastasis occurring at least 1 year later than melanoma diagnosis in BRAF mutated patients, in contrast to nonmutated. In vitro experiments demonstrated that the axis HGF/c-met/Nox4/ROS triggers the epithelial-mesenchymal transition. Conclusions: The observed correlation suggests an interplay between c-met and Nox4 in promoting the onset of metastasis. This study suggests that Nox4 inhibitors could be associated to the current therapy used to treat melanoma patients with BRAF mutations.

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“…Our previous research reported that the abundant expression of CCL18 examined in OSCC could promote the growth and metastasis of cancer cells, and was therefore associated with the TNM stage of oral cancer patients 8 . The metastasis of cancer cells is typically accompanied by a decrease in expression levels of epithelial cell markers (e.g., E-cadherin) and an increase in expression of mesenchymal markers (e.g., N-cadherin, ZEB2, ZEB1, Vimentin, Slug and Twist, among others) 22 , 23 , angiogenesis-related factors (e.g., vascular endothelial growth factor (VEGF)) 24 , and matrix metalloproteinases (e.g., MMP-9 and MMP-2) 25 . The exogenous CCL18 stimulation in OSCC cells was shown to cause a decrease in E-cadherin expression and an increase in N-cadherin and slug expression, suggesting that CCL18 could promote EMT in OSCC cells 26 .…”

Section: Discussionmentioning

confidence: 99%

CCL18-induced LINC00319 promotes proliferation and metastasis in oral squamous cell carcinoma via the miR-199a-5p/FZD4 axis

Jiang

Liu

et al. 2020

Cell Death Dis

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Long non-coding RNAs (lncRNAs), which may be modulated by chemokines, are key regulators in many cancers including oral squamous cell carcinoma (OSCC). An understanding of lncRNAs involved in chemokine (CC motif) ligand 18 (CCL18)-induced OSCC promotion remains elusive. The present study using lncRNA sequencing found LINC00319 to be significantly upregulated in OSCC cells subjected to rCCL18 stimulation. Furthermore, LINC00319 knockdown was found to attenuate the carcinogenic function of CCL18 in OSCC, reducing OSCC proliferation, metastasis, epithelial-mesenchymal transition (EMT), and angiogenesis. LINC00319 was demonstrated to act as a ceRNA in OSCC, which directly responded to miR-199a-5p and rescued the repression of FZD4 by miR-199a-5p. Functionally, in vitro and in vivo experiments showed that LINC00319 promoted OSCC growth and metastasis via downregulating miR-199a-5p and upregulating FZD4. In vitro rescue assays demonstrated that miR-199a-5p inhibitor or FZD4 overexpression reversed the effects of LINC00319 silencing in OSCC. Importantly, the expression of miR-199a-5p and FZD4 were found to be mediated by CCL18, and miR-199a-5p mimics inhibited the CCL18-promoting effects in oral cancer cells. Taken together, these results evidenced a mechanism of CCL18 action in OSCC mediated through the LINC00319/miR-199a-5p/FZD4 signaling pathway, which may comprise a potential target for OSCC therapeutic development.

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Epithelial-Mesenchymal Transition in Skin Cancers: A Review

Cited by 59 publications

References 109 publications

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

The Interplay between HGF/c-met Axis and Nox4 in BRAF Mutated Melanoma

CCL18-induced LINC00319 promotes proliferation and metastasis in oral squamous cell carcinoma via the miR-199a-5p/FZD4 axis

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