MicroRNA-17 induces epithelial-mesenchymal transition consistent with the cancer stem cell phenotype by regulating CYP7B1 expression in colon cancer

Xi, Xiang‐Peng; Zhuang, Jing; Moua, Teng; Xia, Lijian; Yang, Mingyu; Liu, Qing‐Gen; Chen, Jingbo

doi:10.3892/ijmm.2016.2624

Cited by 38 publications

(28 citation statements)

References 43 publications

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“…P values to determine differences in luciferase signal over time were calculated using two-way ANOVA followed by Bonferroni correction of average luciferase signal in each condition. Ã , P < 0.05; ÃÃ , P < 0.01; ÃÃÃ , P < 0.001; ÃÃÃÃ , P < 0.0001. tumor progression (40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51). Importantly, high expression of the Six2-gene signature significantly correlates with a decrease in distant metastasis-free and relapse-free survival across all breast cancer patient samples as well as in TNBC-specific samples ( Fig.…”

Section: Six2 and Sox2 Expression Correlate In Human Breast Cancer Anmentioning

confidence: 87%

SIX2 Mediates Late-Stage Metastasis via Direct Regulation of SOX2 and Induction of a Cancer Stem Cell Program

et al. 2019

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The SIX2/SOX2 axis is critical for promoting metastatic colonization of triple-negative breast cancer cells Survival Self-renewal Metastatic outgrowth Survival Self-renewal Metastatic outgrowth Survival Self-renewal Metastatic outgrowth The capacity for tumor cells to metastasize efficiently is directly linked to their ability to colonize secondary sites. Here we identify Six2, a developmental transcription factor, as a critical regulator of a breast cancer stem cell program that enables metastatic colonization. In several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes associated with embryonic stem cell programs. Six2 directly bound the Sox2 Srr2 enhancer, promoting Sox2 expression and downstream expression of Nanog, which are both key pluripotency factors. Regulation of Sox2 by Six2 enhanced cancer stem cell properties and increased metastatic colonization. Six2 and Sox2 expression correlated highly in breast cancers including TNBC, where a Six2 expression signature was predictive of metastatic burden and poor clinical outcome. Our findings demonstrate that a SIX2/SOX2 axis is required for efficient metastatic colonization, underscoring a key role for stemness factors in outgrowth at secondary sites. Significance: These findings provide novel mechanistic insight into stemness and the metastatic outgrowth of triple-negative breast cancer cells.

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Section: Six2 and Sox2 Expression Correlate In Human Breast Cancer Anmentioning

confidence: 87%

SIX2 Mediates Late-Stage Metastasis via Direct Regulation of SOX2 and Induction of a Cancer Stem Cell Program

et al. 2019

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“…4 They regulate expression of genes at both the transcriptional and posttranscriptional level by binding to the 3′-untranslated region (3′-UTR) of target messenger RNAs (mRNAs), thereby inducing translational repression or mRNA degradation. 6 For example, the miR-17 expression has been observed in breast, 7 nasopharyngeal carcinoma, 8 colon, 9 gastric, 10 ovarian, 11 and lung 12 cancers, and other tumors. 6 For example, the miR-17 expression has been observed in breast, 7 nasopharyngeal carcinoma, 8 colon, 9 gastric, 10 ovarian, 11 and lung 12 cancers, and other tumors.…”

Section: Introductionmentioning

confidence: 99%

miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

Zhao

Sun

et al. 2018

J of Cellular Biochemistry

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MicroRNA‐17‐5p (miR‐17‐5p) and epithelial‐mesenchymal transition (EMT) have been reported to participate in the development and progression of multiple cancers. However, the relationship between the miR‐17‐5p and EMT in osteosarcoma (OS) is still poorly understood. This study was to investigate the effects of the miR‐17‐5p and its potential mechanism in regulating proliferation, apoptosis, and EMT of human OS. Quantitative real‐time PCR was used to detect the miR‐17‐5p and SRC kinase signaling inhibitor 1 (SRCIN1) messenger RNA expression in OS specimens and cell lines. After transfection with miR‐17‐5p inhibitors, proliferation, apoptosis, migration, and invasion of OS cells were assessed by using the Cell Counting Kit‐8, the annexin V‐FITC apoptosis, wound‐healing, and transwell assays. The SRCIN1 was validated as a target of the miR‐17‐5p through bioinformatics algorithms and luciferase reporter assay. Moreover, the expression of EMT markers, E‐cadherin, N‐cadherin, and Snail was identified by the Western blot analysis. MiR‐17‐5p was significantly upregulated in OS tumor samples and cell lines. It inhibited proliferation and EMT, and promoted apoptosis in OS. The SRCIN1 was identified as a direct target of the miR‐17‐5p. Silenced miR‐17‐5p could change the expression of EMT markers, such as upregulating the expression of E‐cadherin, and downregulating the expression of N‐cadherin and Snail through targeting the antioncogenic SRCIN1. These findings suggest that the miR‐17‐5p promotes cell proliferation, and EMT in human OS by directly targeting the SRCIN1, and reveal a branch of the miR‐17‐5p/SRCIN1/EMT signaling pathway involved in the progression of OS.

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“…miRNAs are regulatory RNA molecules in the genome and serve an important role in a number of physiological conditions, including cell differentiation, development, apoptosis, immune response, hematopoiesis, cell death and proliferation (8,9). miRNAs function by binding to complementary sequences on the 3'-untranslated regions, or the open reading frames, of target genes to regulate gene expression at the post-transcriptional level, leading to the degradation of target mRNAs or the inhibition of mRNA translation (10).…”

Section: Function and Mechanisms Of Microrna-20a In Colorectal Cancermentioning

confidence: 99%

Function and mechanisms of microRNA‑20a in colorectal cancer (Review)

et al. 2020

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Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-associated mortality worldwide. CRC currently has no specific biomarkers to promote its diagnosis and treatment and the underlying mechanisms regulating its pathogenesis have not yet been determined. MicroRNAs (miRs) are small, non-coding RNAs that exhibit regulatory functions and have been demonstrated to serve a crucial role in the post-transcriptional regulatory processes of gene expression that is associated with cell physiology and disease progression. Recently, abnormal miR-20a expression has been identified in a number of cancers types and this has become a novel focus within cancer research. High levels of miR-20a expression have been identified in CRC tissues, serum and plasma. In a recent study, miR-20a was indicated to be present in feces and to exhibit a high sensitivity to CRC. Therefore, miR-20a may be used as a marker for CRC and an indicator that can prevent the invasive examination of patients with this disease. Changes in the expression of miR-20a during chemotherapy can be used as a biomarker for monitoring resistance to treatment. In conclusion, miR-20a exhibits the potential for clinical application as a novel diagnostic biomarker and therapeutic target for use in patients with CRC. The present study focused on the role and mechanisms of miR-20a in CRC. Contents 1. Introduction 2. microRNA-20a overview 3. The mechanism of miR-20a in CRC 4. miR-20a can be used as a diagnostic marker in CRC 5. miR-20a may be used as a monitoring indicator during chemotherapy 6. Conclusion and prospects

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MicroRNA-17 induces epithelial-mesenchymal transition consistent with the cancer stem cell phenotype by regulating CYP7B1 expression in colon cancer

Cited by 38 publications

References 43 publications

SIX2 Mediates Late-Stage Metastasis via Direct Regulation of SOX2 and Induction of a Cancer Stem Cell Program

SIX2 Mediates Late-Stage Metastasis via Direct Regulation of SOX2 and Induction of a Cancer Stem Cell Program

miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

Function and mechanisms of microRNA‑20a in colorectal cancer (Review)

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