Substrate stiffness affects epithelial-mesenchymal transition of cervical cancer cells through miR-106b and its target protein DAB2

Piao, Jin-Lan; You, Ke; Guo, Yanli; Zhang, Youyi; Li, Zijian; Geng, Li

doi:10.3892/ijo.2017.3978

Cited by 38 publications

(28 citation statements)

References 31 publications

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“…Cheng et al 15 found that DAB2 is identified as a direct target of miR-106b and it is inhibited by TGF-β1 partly through miR-106b and is involved in TGF-β1-induced CC cell migration. Piao et al 16 reported that miR-106 overexpression and DAB2 knockdown induced epithelial to mesenchymal transition (EMT) of CC cells cultured on substrate. As miR-106b plays an essential role in CC, its molecular mechanisms need to be further studied.…”

Section: Introductionmentioning

confidence: 99%

The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism

Liu

et al. 2018

Cell Death Discov.

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This study aims to investigate the role of miR-106b-5p in cervical cancer by performing a comprehensive analysis on its expression and identifying its putative molecular targets and pathways based on The Cancer Genome Atlas (TCGA) dataset, Gene Expression Omnibus (GEO) dataset, and literature review. Significant upregulation of miR-106b-5p in cervical cancer is confirmed by meta-analysis with the data from TCGA, GEO, and literature. Moreover, the expression of miR-106b-5p is significantly correlated with the number of metastatic lymph nodes. Our bioinformatics analyses show that miR-106b could promote cervical cancer progression by modulating the expression of GSK3B, VEGFA, and PTK2 genes. Importantly, these three genes play a crucial role in PI3K-Akt signaling, focal adhesion, and cancer. Both the expression of miR-106b-5p and key genes are upregulated in cervical cancer. Several explanations could be implemented for this upregulation. However, the specific mechanism needs to be investigated further.

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Section: Introductionmentioning

confidence: 99%

The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism

Liu

et al. 2018

Cell Death Discov.

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“…It has been reported that miR‐106b regulates the EMT of cancer cells and promotes tumor progression . It is also noted that, upon EMT inducement, cancer cells exhibit morphological changes and a couple of EMT‐related molecules including E‐cadherin, vimentin, ck19, Snail, and N‐cadherin.…”

Section: Resultsmentioning

confidence: 99%

“…First, molecular phenotypes of CTCs were associated with various behavior of cancer cells including anoikis resistance metastasis and therapeutic resistance. It has been reported that miR‐106b promotes anoikis resistance and EMT processes in breast cancer cells by targeting RB and Snail gene . Acquisition of a more malignant phenotype for CTC might easily explain the resistance to elimination strategies such as chemotherapy, local antigrowth signaling, and immune attack by the host.…”

Section: Discussionmentioning

confidence: 99%

Incorporating MicroRNA into Molecular Phenotypes of Circulating Tumor Cells Enhances the Prognostic Accuracy for Patients with Metastatic Breast Cancer

et al. 2019

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Background The molecular phenotype of circulating tumor cells (CTCs) was associated with clinical outcome of patients with breast cancer. CTCs isolated from patients with metastatic breast cancer (MBC) display a unique microRNA (miRNA) expression profile. The aim of this study was to enhance the prognostic accuracy of the CTC phenotype in patients with MBC, by incorporating miRNA into a combined prediction model. Subjects, Materials, and Methods CTCs were detected by CellSearch and enriched by magnetic cell sorting. miRNA deep sequencing and quantitative polymerase chain reaction were used to screen and verify potentially CTC‐specific miRNA candidates. Patients with MBC were enrolled from two independent cohorts, and overall survival (OS) and chemotherapy response were analyzed. Results We screened and identified that miR‐106b was an upregulated molecule in patients with MBC with CTC ≥5/7.5 mL (n = 16) compared with patients with CTC = 0/7.5 mL (n = 16) and healthy donors (n = 8). The expression of CTC‐specific miR‐106b correlated with vimentin and E‐cadherin in CTC and acted as an independent factor for predicting OS (hazard ratio 2.157, 95% confidence interval [CI] 1.098–4.239, p = .026). Although CTC‐specific miR‐106b, E‐cadherin, and vimentin showed a prognostic potential independently, the prognostic performance for OS based on the combination of three markers was significantly enhanced in Cohort 1 (area under the curve [AUC] 0.752, 95% CI 0.658–0.847, n = 128) and further validated in Cohort 2 (AUC 0.726, 95% CI 0.595–0.856, n = 91). Besides, a combined model incorporating miR‐106b was associated with therapy response. Conclusion The phenotypic assemblies of CTC incorporating miR‐106b show enhanced prognostic accuracy of overall survival in patients with MBC. Implications for Practice In order to enhance the prognostic accuracy of the circulating tumor cell (CTC) phenotype in patients with metastatic breast cancer (MBC), this study screened and identified a CTC‐specific microRNA (miRNA), miR‐106b, as an upregulated molecule based on the comparison of miRNA profile between CTCs, primary tumors, and healthy blood donors. By incorporating miR‐106b into a combined prediction model, the prognostic accuracy of the CTC phenotype for patients with MBC was greatly improved in both the training and validation cohorts. This work provides clinical evidence supporting the prognostic potential of CTC‐specific miRNA for patients with MBC. These results indicate that developing CTC‐specific miRNAs as new biomarkers will help to further optimize personalized therapy.

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“…Some other literatures have also demonstrated that DAB2 is regulated by various miRNAs at the post‐transcriptional level in multiple cancer types. For instance, miR‐106b is involved in TGFβ1‐induced cell migration by targeting DAB2 in cervical carcinoma . MiR‐93 promotes cell growth and invasion in nasopharyngeal carcinoma by targeting DAB2 .…”

Section: Discussionmentioning

confidence: 99%

miR‐191/DAB2 axis regulates the tumorigenicity of estrogen receptor‐positive breast cancer

Tian

Zhang

2017

IUBMB Life

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Disabled-2 (DAB2) has been shown to be downregulated in a variety of human cancer types including breast tumors. However, the role of DAB2 in estrogen receptor positive (ER+) breast cancer cells has not been reported. In this context, we demonstrated that DAB2 expression was significantly decreased in ER+ breast cancer cell lines and ER+ clinical specimens, compared with ER- breast cancer cell lines and ER- tissues, respectively. Depletion of estrogen significantly elevated DAB2 expression in ER+ MCF7 and T-47D cells. Treatment with estradiol (E2) reduced the expression of DAB2 and administration of tamoxifen upregulated DAB2 expression in a dose-dependent manner. Functionally, silencing of DAB2 in hormone-starved MCF7 and T-47D cells promoted cellular proliferation and enforced expression of DAB2 in normal-cultured or E2-treated cells suppressed cellular proliferation. Mechanistically, estrogen-induced miR-191 was identified as a direct upstream regulator of DAB2 in ER+ cells. Luciferase reporter assay indicated that miR-191 inhibited DAB2 expression by directly targeting the 3'-UTR of DAB2. Importantly, the expression and function of miR-191 showed the opposite tendency with DAB2 in ER+ cells. In vivo, inhibition of miR-191 significantly suppressed the xenograft growth induced by E2, and silencing of DAB2 could restored the growth arrest induced by miR-191 inhibition. Taken together, our data unveil that the miR-191-DAB2 axis seems to be an important pathway associated with estrogen signaling in breast cancer and may serve as a potential diagnostic biomarker and a powerful therapeutic target for ER+ breast cancer patients. © 2017 IUBMB Life, 70(1):71-80, 2018.

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Substrate stiffness affects epithelial-mesenchymal transition of cervical cancer cells through miR-106b and its target protein DAB2

Cited by 38 publications

References 31 publications

The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism

The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism

Incorporating MicroRNA into Molecular Phenotypes of Circulating Tumor Cells Enhances the Prognostic Accuracy for Patients with Metastatic Breast Cancer

miR‐191/DAB2 axis regulates the tumorigenicity of estrogen receptor‐positive breast cancer

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