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Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties

ABSTRACT: Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties

PROVIDER: PRJNA1125448 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29460752.fastq.gz	Fastqsanger.gz
	SRR29460753.fastq.gz	Fastqsanger.gz
	SRR29460754.fastq.gz	Fastqsanger.gz
	SRR29460755.fastq.gz	Fastqsanger.gz
	SRR29460756.fastq.gz	Fastqsanger.gz

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Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties

Project description:Despite advances in breast cancer screening and treatment, prognosis for metastatic disease remains dismal at 30% five-year survival. This is due, in large, to the failure of current therapeutics to target properties unique to metastatic cells. One of the drivers of metastasis is miR-10b, a small noncoding RNA implicated in cancer cell invasion, migration, viability, and proliferation. We have developed a nanodrug termed MN-anti-miR10b that delivers anti-miR10b antisense oligomers to cancer cells. In mouse models of metastatic triple-negative breast cancer, MN-anti-miR10b has been shown to prevent onset of metastasis and eliminate existing metastasis in combination with chemotherapy even after treatment has been stopped. Recent studies have implicated miR-10b in conferring stem cell-like properties onto cancer cells, such as chemoresistance. In this study, we show transcriptional evidence that inhibition of miR-10b with MN-anti-miR10b activates developmental processes in cancer cells and that stem-like cancer cells have increased miR-10b expression. We then demonstrate that treatment of breast cancer cells with MN-anti-miR10b reduces their stemness confirming that these properties make metastatic cells susceptible to the nanodrug actions. Collectively, these findings indicate that inhibition of miR-10b functions to impair breast cancer cell stemness, positioning MN-anti-miR10b as an effective treatment option for stem-like breast cancer subtypes.

2024-09-03 | GSE270229 | GEO

Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties.

Project description:Despite advances in breast cancer screening and treatment, prognosis for metastatic disease remains dismal at 30% five-year survival. This is due, in large, to the failure of current therapeutics to target properties unique to metastatic cells. One of the drivers of metastasis is miR-10b, a small noncoding RNA implicated in cancer cell invasion, migration, viability, and proliferation. We have developed a nanodrug, termed MN-anti-miR10b, that delivers anti-miR-10b antisense oligomers to cancer cells. In mouse models of metastatic triple-negative breast cancer, MN-anti-miR10b has been shown to prevent onset of metastasis and eliminate existing metastases in combination with chemotherapy, even after treatment has been stopped. Recent studies have implicated miR-10b in conferring stem cell-like properties onto cancer cells, such as chemoresistance. In this study, we show transcriptional evidence that inhibition of miR-10b with MN-anti-miR10b activates developmental processes in cancer cells and that stem-like cancer cells have increased miR-10b expression. We then demonstrate that treatment of breast cancer cells with MN-anti-miR10b reduces their stemness, confirming that these properties make metastatic cells susceptible to the nanodrug actions. Collectively, these findings indicate that inhibition of miR-10b functions to impair breast cancer cell stemness, positioning MN-anti-miR10b as an effective treatment option for stem-like breast cancer subtypes.

| S-EPMC11348941 | biostudies-literature

Gene expression profile upon miR-10b overexpression or knockdown

Project description:miR-10b precusor or miR-10b inhibitor was used to overexpress or knockdown miR-10b expression in PANC-1 cells. Microarray analysis was used to characterize the changes in gene expression profiles of PANC-1 upon miR-10b overexpression or knockdown

2015-01-01 | GSE40189 | GEO

Expression analysis for nasopharyngeal carcinoma cell lines (5-8F and 6-10B)

Project description:High metastatic nasopharyngeal carcinoma cell line 5-8F expression patterns against low metastatic nasopharyngeal carcinoma cell line 6-10B.

2009-12-10 | GSE15903 | GEO

Expression analysis for nasopharyngeal carcinoma cell lines (5-8F and 6-10B)

Project description:High metastatic nasopharyngeal carcinoma cell line 5-8F expression patterns against low metastatic nasopharyngeal carcinoma cell line 6-10B. This study was done to screen genes related with metastasis in NPC. The microarray analyses were done in a same batch. 6-10B cells are cultured and harvested at three different time points.

2009-12-10 | E-GEOD-15903 | biostudies-arrayexpress

miRNA sequencing profile of colonic mucosa in global mir-10b KO and WT mice

Project description:Background/ Aim: Diabetes has substantive co-occurrence with disorders of gut-brain interactions (DGBIs). The pathophysiological and molecular mechanisms linking diabetes and DGBIs are unclear. miRNAs are key regulators of diabetes and gut dysmotility. We investigated whether impaired gut barrier function regulated by a key miRNA, miR-10b-5p, links diabetes and gut dysmotility. Methods: We created a new mouse line using the Mb3Cas12a/Mb3Cpf1 endonuclease to knock out mir-10b globally. Loss of function studies were conducted to characterize diabetes, gut dysmotility, and gut barrier dysfunction phenotypes in these mice. Gain of function studies were conducted by injecting these mice with a miR-10b-5p mimic. Further, we performed miRNA-sequencing analysis from colonic mucosa from mir-10b KO, WT, and miR-10b-5p mimic injected mice to confirm 1) deficiency of miR-10b-5p in KO mice, and 2) restoration of miR-10b-5p expression after the mimic injection. Results: Congenital loss of mir-10b in mice led to the development of hyperglycemia, gut dysmotility, and gut barrier dysfunction. We found increased gut permeability and reduced expression of the tight junction protein Zonula occludens-1 (ZO-1), in the colon of mir-10b KO mice. We further confirmed that patients with diabetes or IBS-C, a known DGBI that is linked to leaky gut, had significantly reduced miR-10b-5p expression. Injection of a miR-10b-5p mimic in mir-10b KO mice rescued these molecular alterations and phenotypes. Conclusion: Our study uncovered a potential pathophysiologic mechanism of gut barrier dysfunction that links both the diabetes and gut dysmotility phenotypes in mice lacking miR-10b-5p. Treatment with a miR-10b-5p mimic reversed the leaky gut, diabetic, and gut dysmotility phenotypes, highlighting the translational potential of miR-10b-5p mimic.

2023-07-13 | GSE236981 | GEO

Transcriptome analysis for miR-10b-5p transfected leiomyosarcoma cells

Project description:To investigate the functions of miR-10b-5p in uterine leiomyosarcoma, transcriptome analysis was performed.

2022-06-30 | GSE201542 | GEO

Expression data from U87-2M1 glioma cells transduced with baculoviral control decoy vector or baculoviral miR-10b decoy vector

2012-12-31 | GSE35170 | GEO

Expression data from U87-2M1 glioma cells transduced with baculoviral control decoy vector or baculoviral miR-10b decoy vector

Project description:MicroRNA-10b may target numerous genes in gliomagenesis. The target genes of miR-10b may differ according to the cellular context. We used microarray analyses to determine the phenotypic effects and gene targets of miR-10b by silencing miR-10b in invasive U87-2M1 glioma cells. Early passage U87-2M1 cells treated with the baculoviral control decoy vector or miR-10b decoy vector were selected for RNA extraction and hybridization on microarray

2012-12-31 | E-GEOD-35170 | biostudies-arrayexpress

Oxidative stress-regulatory role of miR-10b-5p in the diabetic human cornea revealed through integrated multi-omics analysis

Project description:The corneal epithelium is maintained by limbal epithelial stem cells (LESCs) and are largely responsible for corneal optical transparency and protection by continuous population of corneal epithelial cells. Diabetes mellitus (DM) has been shown to affect all structures of the eye including the cornea which can result in delayed wound healing and potential vision loss. MicroRNAs (miRNAs) are short non-coding oligonucleotides that regulate various cellular functions, including oxidative stress response, by repressing translation. miR-10b-5p was previously identified to be upregulated in diabetic vs. non-diabetic limbal cells and our purpose was to understand the role of miR-10b-5p in human limbal epithelial cells in normal and pathological conditions such as diabetes mellitus. It was hypothesized that miR-10b-5p influences corneal epithelial homeostasis by modulating antioxidant defenses and wound healing processes. Through integrated transcriptomic and proteomic analyses, we identified GCLM and LANCL1 as key miR-10b-5p targets, revealing its profound impact on glutathione metabolism, sulfur compound biosynthesis processes, and antioxidant defenses. Our finding suggests that miR-10b suppression disrupts redox balance which potentially leads to heightened oxidative stress, impaired wound healing and increased cellular vulnerability in diabetic corneas. Further research into miR-10b inhibitors or gene modulation strategies may pave the way for novel treatments aimed at mitigating oxidative stress-related corneal dysfunction, particularly in diabetes-induced ocular diseases.

2025-07-01 | GSE292721 | GEO

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