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MiR-4711-5p regulates the cancer stemness and cell cycle progression through direct binding to KLF5, MDM2 and TFDP1 in colon cancer cells

ABSTRACT: miR-4711-5p regulates the cancer stemness and cell cycle progression through direct binding to KLF5, MDM2 and TFDP1 in colon cancer cells

PROVIDER: PRJNA555420 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9700080.fastq.gz	Fastqsanger.gz
	SRR9700081.fastq.gz	Fastqsanger.gz
	SRR9700078.fastq.gz	Fastqsanger.gz
	SRR9700079.fastq.gz	Fastqsanger.gz

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miR-4711-5p regulates the cancer stemness and cell cycle progression through direct binding to KLF5, MDM2 and TFDP1 in colon cancer cells

Project description:It is important to establish cancer stem cells (CSCs)-targeted therapy for eradication of cancer. In this study, we searched for candidate microRNAs (miRNAs) by in silico analyses, which inhibit a stem cell-related gene Krüppel-like factor 5 (KLF5). After in vitro screening we focused on miR-4711-5p which proved to inhibit cancer stemness and G1-S cell cycle progression. We found by luciferase binding assays that miR-4711-5p directly bound to KLF5, TFDP1 (a heterodimeric partner with E2F family), and MDM2 (one responsible gene for degradation of wild type p53). This miRNA suppressed cell proliferation, migration, and invasion ability in DLD-1 and HCT116 cells as well as the cancer stemness including low reactive oxygen species (ROS) activity, and sphere formation ability. The expressions of stem cell markers, LGR5, CD44v9, and BMI1 also decreased. MiR-4711-5p inhibited the in vivo growth of pre-established DLD-1 xenografts without apparent adverse effect. RNA sequence Analyses indicated that the transition from G1 phase to S phase in cell cycle was disturbed by miR-4711-5p. We indeed found that miR-4711-5p provoked G1 arrest with increase in CDK inhibitor p27KIP1 and/or p21WAF1/CIP1 and decrease in CDK2, 4, 6 and Cyclin D1 protein expression. These changes could be attributed to direct binding of miR-4711-5p to TFDP1. It is also suggested that down-regulation of MDM2 could permit to accumulate the wild type p53 protein in HCT116, leading to drastic induction of the p21WAF1/CIP1 protein and apoptosis. Our data suggest that miR-4711-5p could be a hopeful next generation treatment for CSC-targeted therapy.

2020-02-19 | GSE134442 | GEO

miR-4711-5p regulates cancer stemness and cell cycle progression via KLF5, MDM2 and TFDP1 in colon cancer cells.

Project description:BackgroundIt is important to establish cancer stem cell (CSC)-targeted therapies to eradicate cancer. As it is a CSC marker, we focused on Kruppel-like factor 5 (KLF5) in this study.MethodsWe searched for candidate microRNAs (miRNAs) that inhibited KLF5 expression by in silico analyses and screened them in colon cancer cell lines.ResultsWe identified one promising miRNA, miR-4711-5p, that downregulated KLF5 expression by direct binding. This miRNA suppressed cell proliferation, migration and invasion ability, as well as stemness, including decreased stem cell marker expression, reactive oxygen species activity and sphere formation ability. MiR-4711-5p inhibited the growth of DLD-1 xenografts in nude mice with no adverse effects. We found that miR-4711-5p provoked G1 arrest, which could be attributed to direct binding of miR-4711-5p to TFDP1 (a heterodimeric partner of the E2F family). Our findings also suggested that direct binding of miR-4711-5p to MDM2 could upregulate wild-type p53, leading to strong induction of apoptosis. Finally, we found that miR-4711-5p had a potent tumour-suppressive effect compared with a putative anti-oncomiR, miR-34a, in tumour cell cultures derived from five patients with colorectal cancer.ConclusionsOur data suggest that miR-4711-5p could be a promising target for CSC therapy.

| S-EPMC7109136 | biostudies-literature

KLF5 promotes stemness and PARPi resistance through regulation of Vimintin in ovarian cancer

Project description:To investigate the function of KLF5 in ovarian cancer, we established SKOV3 cell lines in which KLF5 has been knocked down by shRNA.Cells were collected and performed RNA sequencing.

2024-05-01 | GSE248659 | GEO

KLF5 promotes stemness and PARPi resistance through regulation of Vimintin in ovarian cancer

Project description:KLF5 promotes stemness and PARPi resistance through regulation of Vimintin in ovarian cancer

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Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers

Project description:The transcription factor KLF5 is highly expressed in basal-like breast cancer (BLBC). It promotes cell proliferation, survival, migration and stemness and serves as a potential therapeutic target. In this study, we first identified a super-enhancer (SE) located downstream of the KLF5 gene in BLBC. JQ-1, a BRD4-bromodomain inhibitor, inhibits the expression and activity of KLF5 in the HCC1806 and HCC1937 cell lines in time- and dose-dependent manners. A new BRD4 inhibitor, compound 870, is more potent than JQ-1 in terms of its ability to inhibit KLF5 and BLBC growth by inducing G1 phase cell cycle arrest. Additionally, a CDK7 inhibitor, THZ1, also inhibits KLF5 and BLBC growth. Our findings suggested that SE regulates KLF5 and that SE inhibitors could be an effective therapeutic strategy for treating BLBC.

2019-10-01 | GSE124748 | GEO

Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

Project description:To identify which genes are regulated by KLF5 and its acetylation, we performed RNA-Seq and bioinformatics analyses in KLF5-null prostate cancer cells expressing KLF5, KLF5KR, and KLF5KQ.

2020-12-19 | GSE161950 | GEO

Over-expression and knockdown of KLF5

Project description:Activation of the Ras/Erk pathway upregulates expression of the Kruppel-like Factor 5 (KLF5) transcription factor, and KLF5 is a downstream mediator of Ras oncogenic signaling. Specifically, in bladder and colon cancer cell lines KLF5 upregulates the Ras-pathway target gene cyclin D1, and facilitates entry into the S phase of the cell cycle. Ras mutations are common in lung cancer, but a role for KLF5 in lung tumorigenesis has not been defined. To this end, we manipulated KLF5 expression in four Ras-mutant human lung adenocarcinoma cell lines to find that KLF5 significantly modulates anchorage-independent growth, a mutant Ras phenotype. However, in a mouse model of human lung adenocarcinoma, K-RasG12D does not critically require Klf5 to mediate oncogenesis or induce cyclin D1 expression. Patients with lung tumors expressing high levels of KLF5 have significantly better prognosis than those with low or no KLF5 expression (opposite of mutant Ras prognosis). The latter may be explained by KLF5 transcriptional repression of the ATP-binding cassette, sub-family G (WHITE), member 2 (ABCG2), an anthracycline transporter. In agreement with this, KLF5 knockdown cells display significantly more Hoechst “side population” and resistance to doxorubicin. In summary, while KLF5 is not an obligate partner in Ras oncogenic signaling, KLF5 control of ABCG2 expression is significant to patient survival.

2010-06-23 | GSE16555 | GEO

Different forms of KLF5 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

Project description:To identify which genes are directly regulated by KLF5 and its acetylation, we performed ChIP-Seq and bioinformatics analyses in KLF5-null prostate cancer cells expressing KLF5, KLF5KR, and KLF5KQ.

2020-12-19 | GSE161949 | GEO

ChIP-seq of patient derived colorectal cancer cell lines using KLF5 and H3K27 acetylation

Project description:Discovery of genome-wide KLF5 binding sites in the PDCs. Chromatin was obtained from colorectal cancer cell line of one patient, and subjected to ChIP-seq using KLF5, H3K27 antibodies prepared using the NEB Next® ChIP-Seq Library kit (NEB Biolabs) according to the manufacturer’s instructions, and sequenced using the HiSeq 2000 system (Illumina). Raw data from input, KLF5 and H3K27 are uploaded.

2022-12-24 | E-MTAB-8080 | biostudies-arrayexpress

Cancer-associated fibroblasts promote the stemness and progression of renal cell carcinoma via exosomal miR-181d-5p

Project description:The mechanisms underlying the effects of cancer-associated fibroblasts (CAFs) on cancer stemness and tumor progression in renal cell carcinoma (RCC) have not been elucidated yet. In the present study, we found that the enrichment of CAFs was positively associated with tumor progression and cancer stemness in RCC. Further investigation revealed that CAFs could enhance cancer stemness through delivering exosomes to RCC cells, and miR-181d-5p was identified as the critical exosomal miRNA in CAF secreted exosomes by small RNA sequencing and subsequent screening assays. Mechanistically, exosomal miR-181d-5p transferred from CAFs to RCC cells directly suppressed the expression of ring finger protein 43 (RNF43) and activated Wnt/β-catenin signaling pathway, thus promoted cancer stemness and tumor progression. Overexpression of RNF43 strongly suppressed stemness properties and the effects could be reverted by miR-181d-5p. Overall, our findings revealed a crucial mechanism by which CAFs secreted exosomal miRNAs to enhance cancer stemness and thus promote RCC progression, suggesting a new avenue based on CAF secreted miRNAs for more effective targeted therapies.

2022-11-09 | GSE213453 | GEO

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