The interplay between microRNAs and Twist1 transcription factor: a systematic review

Khanbabaei, Hashem; Teimoori, Ali; Mohammadi, Milad

doi:10.1007/s13277-016-4960-y

Cited by 27 publications

(17 citation statements)

References 94 publications

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“…Thus, our findings establish a previously unrecognized and important role for TWIST1 in the recurrence of different stages of LAD patients and malignant progression. TWIST1 functions as a negative regulator of epithelial gene expression and a positive regulator of mesenchymal gene expression, leading to induction of the EMT (15,27). In this study, TWIST1 was found to be upregulated in two LAD cell lines after hypoxic induction.…”

Section: Discussionmentioning

confidence: 50%

“…TWIST1, a basic-helix-loop-helix (bHLH) transcription factor, is one of the most important EMT-inducer prototypes (14). TWIST1 binds to the E-box elements of E-cadherin TWIST1 upregulates miR-214 to promote epithelial-to-mesenchymal transition and metastasis in lung adenocarcinoma and represses its expression, whereas it promotes N-cadherin expression by binding to the E-box elements of N-cadherin (15). In addition, TWIST1 regulates the expression of miRNAs.…”

Section: Introductionmentioning

confidence: 99%

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TWIST1 upregulates miR-214 to promote epithelial-to-mesenchymal transition and metastasis in lung adenocarcinoma

et al. 2018

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Epithelial-to-mesenchymal transition (EMT) is essential for the progression of non-invasive tumor cells into malignancy and metastasis. We found that miR-214 was increased in lung adenocarcinoma (LAD) and positively associated with metastasis, which was mediated by EMT. However, the mechanism whereby the overexpression of microRNAs (miRNAs), such as miR-214, promote EMT in LAD remains unclear. In this study, we found that TWIST1, an independent prognostic factor for overall survival, was increased in LAD and correlated positively with LAD recurrence and progression. We also found that TWIST1 contributes to the EMT process and metastasis of LAD cells. Most importantly, a positive correlation was found between the expression of miR-214 and TWIST1 in clinical LAD tissue. Additionally, miR-214 expression was decreased and its target gene suppressor of fused homolog (SUFU) was increased in LAD cells in response to the impairment of TWIST1 expression by shRNA. Overall, this study provides the first evidence to show that the high expression of TWIST1 increases the expression of miR-214 to promote the EMT process and metastasis in LAD. These findings contribute to clarify the mechanisms whereby miRNAs regulate the EMT process and implicate a new TWIST1-miR-214 pathway in the control of migration and invasion of LAD.

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Section: Discussionmentioning

confidence: 50%

Section: Introductionmentioning

confidence: 99%

TWIST1 upregulates miR-214 to promote epithelial-to-mesenchymal transition and metastasis in lung adenocarcinoma

et al. 2018

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“…Moreover, it was shown that Twist plays a key role in various aspects of tumorigenesis such as tumor initiation, stemness, angiogenesis, metastasis, and drug resistance. 8,41 F I G U R E 6 The schematic model of FR effects on the induction of EMT and radioresistance phenotypes. FR could promote EMT phenotype in relatively invasive cell lines but not in low invasive or noninvasive cell lines.…”

Section: Discussionmentioning

confidence: 99%

Fractionated radiotherapy might induce epithelial‐mesenchymal transition and radioresistance in a cellular context manner

Tahmasebi-Birgani

Teimoori

Ghadiri

et al. 2018

J of Cellular Biochemistry

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Despite the fact that radiotherapy is a main therapeutic modality in cancer treatment, recent evidence suggests that fractionated radiotherapy (FR) might confer radioresistance through epithelial‐mesenchymal transition (EMT). Nevertheless, the effects of FR on EMT phenotype and the potential link between EMT induction and radioresistance development yet to be clarified. The aim of this study was to assess whether FR could promote EMT, and to elucidate if induction of EMT contributes to the acquisition of radioresistance. To this end, two human cancer cell lines (A549 and HT‐29) were irradiated (2 Gy/day) and analyzed using wound healing, transwell migration and invasion assays, real‐time polymerase chain reaction (for E‐cadherin, N‐cadherin, Vimentin, CD44, CD133, Snail, and Twist), clonogenic assay, Annexin V/PI, and 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5 diphenyl tetrazolium bromide (MTT) assay. Irradiation of A549 (for 5 or 10 consecutive days) resulted in morphological changes including elongation of cytoplasm and nuclei and pleomorphic nuclei. Also, irradiation‐enhanced migratory and invasive potential of A549. These phenotypic changes were in agreement with decreased expression of the epithelial marker (E‐cadherin), enhanced expression of mesenchymal markers (N‐cadherin, Vimentin, Snail, and Twist) and increased stemness factors (CD44 and CD133). Moreover, induction of EMT phenotype was accompanied with enhanced radioresistance and proliferation of irradiated A549. However, FR (for 5 consecutive days) did not increase HT‐29 motility. Furthermore, molecular alterations did not resemble EMT phenotype (downregulation of E‐cadherin, Vimentin, ALDH, CD44, CD133, and Snail). Eventually, FR led to enhanced radiosensitivity and decreased proliferation of HT‐29. Altogether, our findings suggest that FR might induce EMT and confer radioresistance in a cell context‐dependent manner.

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“…Although multiple miRNAs ( miR-33a , miR-106a/b and miR-214 ) have been reported to regulate TWIST1 [35], this is the first study to show that miR-210-3p directly regulates TWIST1 expression. Also, the TCGA cohort analysis showed a negative correlation between the expression of TWIST1 and miR-210-3p .…”

Section: Discussionmentioning

confidence: 99%

microRNA-210-3p depletion by CRISPR/Cas9 promoted tumorigenesis through revival of TWIST1 in renal cell carcinoma

et al. 2017

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Previous studies showed that five miRNAs (miR-885-5p, miR-1274, miR-210-3p, miR-224 and miR-1290) were upregulated the most in clear cell renal cell carcinoma (ccRCC). Our focus was to understand from a clinical standpoint the functional consequences of upregulating miR-210-3p. Towards this, we utilized the CRISPR/Cas9 gene editing system to deplete miR-210-3p in RCC cell lines (786-o, A498 and Caki2) and characterized the outcomes. We observed that miR-210-3p depletion dramatically increased tumorigenesis, including altering the morphology of A498 and Caki2 cells in a manner characteristic of epithelial-mesenchymal transition (EMT). These results were corroborated by in vivo xenograft studies, which showed enhanced growth of tumors from miR-210-3p-depleted A498 cells. We identified Twist-related protein 1 (TWIST1) as a key target of miR-210-3p. Analysis of the ccRCC patient data in The Cancer Genome Atlas database showed a negative correlation between miR-210-3p and TWIST1 expression. High TWIST1 and low miR-210-3p expression associated with poorer overall and disease-free survival as compared to low TWIST1 and high miR-210-3p expression. These findings suggest that renal cell carcinoma progression is promoted by TWIST1 suppression mediated by miR-210-3p.

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The interplay between microRNAs and Twist1 transcription factor: a systematic review

Cited by 27 publications

References 94 publications

TWIST1 upregulates miR-214 to promote epithelial-to-mesenchymal transition and metastasis in lung adenocarcinoma

TWIST1 upregulates miR-214 to promote epithelial-to-mesenchymal transition and metastasis in lung adenocarcinoma

Fractionated radiotherapy might induce epithelial‐mesenchymal transition and radioresistance in a cellular context manner

microRNA-210-3p depletion by CRISPR/Cas9 promoted tumorigenesis through revival of TWIST1 in renal cell carcinoma

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