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MicroRNA-30c inhibits Human Breast Tumor Chemotherapy Resistance by regulating TWF1 and IL-11: Patient DataSet

ABSTRACT: Chemotherapy resistance frequently drives tumor progression. However, the underlying molecular mechanisms are poorly characterized. Epithelial-to-mesenchymal transition (EMT) has been shown to correlate with therapy resistance, but the functional link and signaling pathways remain to be elucidated. We report here that miR-30c, a human breast tumor prognostic marker, plays a pivotal role in chemo-resistance by a direct targeting of the actin-transporter TWF1, which promotes EMT. An IL-6 family member, IL-11 was identified as a secondary target of TWF1 in the miR-30c signaling pathway. Expression of miR-30c inversely correlated with IL-11 expression in clinical tumors and IL-11 correlated with relapse-free survival in breast cancer patients. Identification of a novel miRNA-mediated pathway that regulates chemo-resistance in breast cancer will facilitate the development of new management strategies. reference x sample

ORGANISM(S): Homo sapiens

SUBMITTER: Perou Charles

PROVIDER: S-ECPF-GEOD-22049 | biostudies-other |

REPOSITORIES: biostudies-other

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MicroRNA-30c inhibits Human Breast Tumor Chemotherapy Resistance by regulating TWF1 and IL-11: Patient DataSet

Project description:Chemotherapy resistance frequently drives tumor progression. However, the underlying molecular mechanisms are poorly characterized. Epithelial-to-mesenchymal transition (EMT) has been shown to correlate with therapy resistance, but the functional link and signaling pathways remain to be elucidated. We report here that miR-30c, a human breast tumor prognostic marker, plays a pivotal role in chemo-resistance by a direct targeting of the actin-transporter TWF1, which promotes EMT. An IL-6 family member, IL-11 was identified as a secondary target of TWF1 in the miR-30c signaling pathway. Expression of miR-30c inversely correlated with IL-11 expression in clinical tumors and IL-11 correlated with relapse-free survival in breast cancer patients. Identification of a novel miRNA-mediated pathway that regulates chemo-resistance in breast cancer will facilitate the development of new management strategies. reference x sample

2013-01-18 | E-GEOD-22049 | biostudies-arrayexpress

MicroRNA-30c inhibits Human Breast Tumor Chemotherapy Resistance by regulating TWF1 and IL-11: Patient DataSet

2013-01-18 | GSE22049 | GEO

MicroRNA-30c inhibits Human Breast Tumor Chemotherapy Resistance by regulating TWF1 and IL-11: MDA-MB231 DataSet

| S-ECPF-GEOD-32617 | biostudies-other

MicroRNA-30c inhibits human breast tumour chemotherapy resistance by regulating TWF1 and IL-11.

Project description:Chemotherapy resistance frequently drives tumour progression. However, the underlying molecular mechanisms are poorly characterized. Epithelial-to-mesenchymal transition has been shown to correlate with therapy resistance, but the functional link and signalling pathways remain to be elucidated. Here we report that microRNA-30c, a human breast tumour prognostic marker, has a pivotal role in chemoresistance by a direct targeting of the actin-binding protein twinfilin 1, which promotes epithelial-to-mesenchymal transition. An interleukin-6 family member, interleukin-11 is identified as a secondary target of twinfilin 1 in the microRNA-30c signalling pathway. Expression of microRNA-30c inversely correlates with interleukin-11 expression in primary breast tumours and low interleukin-11 correlates with relapse-free survival in breast cancer patients. Our study demonstrates that microRNA-30c is transcriptionally regulated by GATA3 in breast tumours. Identification of a novel microRNA-mediated pathway that regulates chemoresistance in breast cancer will facilitate the development of novel therapeutic strategies.

| S-EPMC3723106 | biostudies-literature

MicroRNA-30c inhibits Human Breast Tumor Chemotherapy Resistance by regulating TWF1 and IL-11: MDA-MB231 DataSet

2013-01-18 | E-GEOD-32617 | biostudies-arrayexpress

MicroRNA-30c inhibits Human Breast Tumor Chemotherapy Resistance by regulating TWF1 and IL-11: MDA-MB231 DataSet

2013-01-18 | GSE32617 | GEO

MicroRNA-30c inhibits pancreatic cancer cell proliferation by targeting twinfilin 1 and indicates a poor prognosis.

Project description:BACKGROUND:Studies have reported that microRNA-30c (miR-30c) has vital functions in the development and progression of multiple cancers. AIM:To investigate the clinical significance and role of miR-30c in pancreatic cancer. METHODS:MiR-30c and twinfilin 1 (TWF1) expression levels were analyzed in Gene Expression Omnibus datasets and validated in human pancreatic cancer by quantitative real-time polymerase chain reaction (RT-qPCR). The effects of miR-30c on pancreatic cancer cell growth, apoptosis, and cell cycle were evaluated by CCK-8 and flow cytometry assays. Furthermore, the in vivo effects were investigated using a subcutaneous xenograft experiment. Target gene prediction software and luciferase reporter assays were used to identify TWF1 as a direct target of miR-30c. RESULTS:The expression of miR-30c was significantly decreased in pancreatic cancer tissues and associated with survival. Gain- and loss-of-function assays showed that miR-30c suppressed pancreatic cancer cell proliferation in vitro and in vivo. RT-qPCR, Western blot, and luciferase reporter assays showed that miR-30c directly targeted TWF1. The expression level of miR-30c was negatively correlated with TWF1 expression in pancreatic cancer tissues. Furthermore, the effects of ectopic miR-30c were rescued by TWF1 overexpression. CONCLUSION:Our results identified the role of the miR-30c/TWF1 axis in pancreatic cancer progression and demonstrated that miR-30c might serve as a prognostic biomarker and therapeutic target for pancreatic cancer.

| S-EPMC6861845 | biostudies-literature

Role of MicroRNA-30c in cancer progression.

Project description:MicroRNAs (miRNAs or miRs) is a non-coding small RNA of a type of 18~24 nucleotide-regulated gene that has been discovered in recent years. It mainly degrades the target gene mRNA or inhibits its translation process through the complete or incomplete bindings with 3'UTR of target genes, followed by the regulation of individual development, apoptosis, proliferation, differentiation and other life activities through the post-transcriptional regulation. Among many miRNAs, the microRNA family, miR-30, plays diverse roles in these key process of neoplastic transformation, metastasis, and clinical outcomes in different cancer progression. As key member of miR-30, miR-30c is regulated by oncogenic transcription factors and cancer progression related genes. Recently, numerous studies have demonstrated that the aberrant expression of miR-30c was significantly associated with the majority of human cancer progression. In this review, the diverse roles of miR-30c in different cancer progression such as the cellular and molecular mechanisms, the potential applications in clinics were summarized to speculate the benefits of miR-30c over-expression in cancer treatment and prognosis.

| S-EPMC7066027 | biostudies-literature

Long non-coding RNA-X-inactive specific transcript inhibits cell viability, and induces apoptosis through the microRNA-30c-5p/Bcl2-like protein 11 signaling axis in human granulosa-like tumor cells.

Project description:The role of long noncoding RNAs (lncRNAs) is being actively explored in polycystic ovary syndrome (PCOS). Recent research has shown that long non-coding RNA (lncRNA) X-inactive Specific Transcript (XIST) is overexpressed in patients with PCOS and is associated with poor pregnancy outcomes. However, the precise function and mechanism of action of lncRNA XIST in PCOS are unknown. We aimed to determine whether lncRNA XIST contributes to PCOS by modulating ovarian granulosa cell physiology. We also investigated any potential molecular regulatory mechanisms. In this study, we discovered that the lncRNA XIST was significantly downregulated in human ovarian granulosa-like tumor (KGN) cells. Notably, overexpression of lncRNA XIST decreased miR-30c-5p expression in KGN cells, inhibited proliferation, and induced apoptosis in KGN cells. However, cotransfection with amiR-30c-5p mimic significantly reduced these effects. Additionally, we discovered that the miR-30c-5p mimic effectively inhibited Bcl2-like protein 11 (BCL2L11) expression, a critical apoptotic promoter, whereas silencing of miR-30c-5p increased BCL2L11 expression, inhibited KGN cell proliferation, and induced apoptosis. In contrast, cotransfection of BCL2L11 with siRNA significantly reversed these effects. In conclusion, this study established that lncRNA XIST plays a critical role in PCOS by modulating the miR-30c-5p/BCL2L11 signaling axis and regulating ovarian granulosa cell physiology.

| S-EPMC9342309 | biostudies-literature

MicroRNA-30c-regulated HDAC9 mediates chemoresistance of breast cancer.

Project description:PurposeAlthough histone deacetylase (HDAC) inhibitors have been shown to effectively induce the inhibition of proliferation and migration in breast cancer, the mechanism of HDAC9's contribution to chemoresistance remains poorly understood. The aim of this study was to investigate the role of miR-30c-regulated HDAC9 in chemoresistance of breast cancer and to determine the potential of selective inhibition of HDAC9 in sensitizing resistant breast cancer cells to chemotherapy.MethodsExpression levels of HDAC9 and miR-30c were measured in breast cancer cells and tissues using quantitative PCR analysis. The effect of selective inhibition of HDAC9 on sensitizing MDR cells to chemotherapy was assessed. MiR-30c/HDAC9 pathways' potential to mediate chemoresistance was analyzed.ResultsOur studies show that HDAC9 was significantly up-regulated in chemoresistant breast cancer cell lines compared to a chemosensitive cell line and was inversely correlated with the levels of miR-30c. MiR-30c mimics and HDAC9 inhibitors reversed the chemoresistance of multidrug-resistant breast cancer cells.ConclusionsThese results indicate that the mechanism of chemoresistance reversal with selective HDAC inhibition was partially realized by regulating miR-30c via directly targeting HDAC9. Our findings suggest that the miR-30c/HDAC9 signaling axis could be a novel and potential therapeutic target in chemoresistant breast cancer.

| S-EPMC7021558 | biostudies-literature

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