scholarly journals Retraction Note: MicroRNA-27a-3p Modulates the Wnt/β-Catenin Signaling Pathway to Promote Epithelial-Mesenchymal Transition in Oral Squamous Carcinoma Stem Cells by Targeting SFRP1

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bin Qiao ◽  
Bao-Xia He ◽  
Jing-Hua Cai ◽  
Qian Tao ◽  
Alfred King-yin Lam
Keyword(s):  
Stem Cells ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Squamous Carcinoma ◽  
Mesenchymal Transition ◽  
Link Type ◽  
Oral Squamous Carcinoma

Editor's Note: this Article has been retracted; the Retraction Note is available at https://www.nature.com/articles/s41598-020-77203-x

scholarly journals RETRACTED ARTICLE: MicroRNA-27a-3p Modulates the Wnt/β-Catenin Signaling Pathway to Promote Epithelial-Mesenchymal Transition in Oral Squamous Carcinoma Stem Cells by Targeting SFRP1

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Bin Qiao ◽  
Bao-Xia He ◽  
Jing-Hua Cai ◽  
Qian Tao ◽  
Alfred King-yin Lam
Keyword(s):  
Stem Cells ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Squamous Carcinoma ◽  
Luciferase Reporter ◽  
Mesenchymal Transition ◽  
Oral Squamous Carcinoma ◽  
Related Proteins ◽  
Emt Markers ◽  
E Cadherin

AbstractThis study aimed to elucidate how microRNA27a-3p (miR-27a-3p) modulates the Wnt/β-catenin signaling pathway to promote the epithelial-mesenchymal transition (EMT) in oral squamous carcinoma stem cells (OSCSCs) by targeting secreted frizzled-related protein 1 (SFRP1). Flow cytometry was used to sort OSCSCs from the SCC-9 and Tca8113 cell lines. The OSCSCs were randomly assigned into the miR-27a-3p inhibitors group, the miR-27a-3p inhibitors-NC group, the si-SFRP1 group, the si-SFRP1 + miR-27a-3p inhibitors group and the blank group. A luciferase reporter, immunofluorescence and Transwell assays were performed to detect luciferase activity, SFRP1, and cell migration and invasion, respectively. The mRNA expression of miR-27a-3p, SFRP1 and EMT markers (E-cadherin, N-cadherin, vimentin and ZEB1) were detected using qRT-PCR. The protein expression of SFRP1, EMT markers and the proteins of the Wnt/β-catenin signaling pathway was detected by Western blotting. OSCSCs showed up-regulated miR-27a-3p, Wnt/β-catenin signaling pathway-related proteins, vimentin, N-cadherin and ZEB1 and down-regulated SFRP1 and E-cadherin. MiR-27a-3p targeted SFRP1. Down-regulated miR-27a-3p resulted in increased E-cadherin and SFRP1 but decreased vimentin, N-cadherin, ZEB1, the Wnt/β-catenin signaling pathway-related proteins, and invasive and migratory cells. Silenced SFRP1 reversed this effect. We found that miR-27a-3p modulated the Wnt/β-catenin signaling pathway to promote EMT in OSCSCs by down-regulating SFRP1.

scholarly journals Detection of cancer stem cells by EMT-specific biomarker-based peptide ligands

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yi-An Chen ◽  
Cheau-Ling Ho ◽  
Min-Tzu Ku ◽  
Luen Hwu ◽  
Cheng-Hsiu Lu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Epithelial Mesenchymal Transition ◽  
Squamous Carcinoma ◽  
Peptide Ligands ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Human Tongue ◽  
Molecule Inhibitor ◽  
Squamous Carcinoma Cell

AbstractThe occurrence of epithelial-mesenchymal transition (EMT) within tumors, which enables invasion and metastasis, is linked to cancer stem cells (CSCs) with drug and radiation resistance. We used two specific peptides, F7 and SP peptides, to detect EMT derived cells or CSCs. Human tongue squamous carcinoma cell line-SAS transfected with reporter genes was generated and followed by spheroid culture. A small molecule inhibitor-Unc0642 and low-dose ionizing radiation (IR) were used for induction of EMT. Confocal microscopic imaging and fluorescence-activated cell sorting analysis were performed to evaluate the binding ability and specificity of peptides. A SAS xenograft mouse model with EMT induction was established for assessing the binding affinity of peptides. The results showed that F7 and SP peptides not only specifically penetrated into cytoplasm of SAS cells but also bound to EMT derived cells and CSCs with high nucleolin and vimentin expression. In addition, the expression of CSC marker and the binding of peptides were increased in tumors isolated from Unc0642/IR-treated groups. Our study demonstrates the potential of these peptides for detecting EMT derived cells or CSCs and might provide an alternative isolation method for these subpopulations within the tumor in the future.

MicroRNA-378-3p/5p suppresses the migration and invasiveness of oral squamous carcinoma cells by inhibiting KLK4 expression

2020 ◽  
Vol 98 (2) ◽  
pp. 154-163
Author(s):  
Zhi Cui ◽  
Shiqun Sun ◽  
Qilin Liu ◽  
Xuechun Zhou ◽  
Siyu Gao ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Squamous Carcinoma ◽  
Effective Measure ◽  
Mesenchymal Transition ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma ◽  
In Cells

Distant metastasis frequently occurs in oral squamous cell carcinoma (OSCC) and contributes to the adverse prognosis for patients with OSCC. However, the potential mechanisms behind the metastasis have not yet been clarified. This study investigated the role of miR-378 in the migration and invasiveness of OSCC in vitro and in vivo. According to our results, the migration and invasiveness of OSCC cells were increased in cells overexpressing miR-378, and reduced in cells where miR-378-3p/5p was silenced. In addition, overexpression of miR-378 suppressed the expressions and activities of matrix metalloproteinase 9 (MMP-9) and MMP-2. Epithelial–mesenchymal transition (EMT) was restrained by overexpression of miR-378, as evidenced by an increase in E-cadherin expression and decrease in N-cadherin and uPA expression. However, knockdown of miR-378-3p/5p produced the opposite results. Moreover, kallikrein-related peptidase 4 (KLK4) was confirmed to be a target gene of miR-378. Overexpression of KLK4 reversed the induced decrease in migration and invasiveness of cells overexpressing miR-378 by upregulating the levels of MMP-9, MMP-2, and N-cadherin, and downregulating the level of E-cadhrin. Finally, the number of metastasis nodules in the lung tissues of nude mice was reduced by overexpression of miR-378, whereas the number of metastases increased with knockdown of miR-378. Taken together, our results suggest that the miR-378–KLK4 axis is involved in the mechanisms behind the migration and invasiveness of OSCC cells. Targeting the miR-378–KLK4 axis may be an effective measure for treating OSCC.

scholarly journals Snail-dependent and -independent Epithelial-Mesenchymal Transition in Oral Squamous Carcinoma Cells

2006 ◽  
Vol 54 (11) ◽  
pp. 1263-1275 ◽  
Author(s):  
Minna Takkunen ◽  
Reidar Grenman ◽  
Mika Hukkanen ◽  
Matti Korhonen ◽  
Antonio García de Herreros ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

scholarly journals Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 217 ◽  
Author(s):  
Wook Jin
Keyword(s):  
Stem Cells ◽  
Tumor Microenvironment ◽  
Cancer Stem Cells ◽  
Signaling Pathway ◽  
Essential Role ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

The JAK/STAT3 signaling pathway plays an essential role in various types of cancers. Activation of this pathway leads to increased tumorigenic and metastatic ability, the transition of cancer stem cells (CSCs), and chemoresistance in cancer via enhancing the epithelial–mesenchymal transition (EMT). EMT acts as a critical regulator in the progression of cancer and is involved in regulating invasion, spread, and survival. Furthermore, accumulating evidence indicates the failure of conventional therapies due to the acquisition of CSC properties. In this review, we summarize the effects of JAK/STAT3 activation on EMT and the generation of CSCs. Moreover, we discuss cutting-edge data on the link between EMT and CSCs in the tumor microenvironment that involves a previously unknown function of miRNAs, and also discuss new regulators of the JAK/STAT3 signaling pathway.

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