ArticleRNA biology2014
Identification of miRNAs that specifically target tumor suppressive KLF6-FL rather than oncogenic KLF6-SV1 isoform.
Article in RNA biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Alternative Splicing in Tumorigenesis and Cancer Therapy.Biomolecules · 2025Review
- Non-Coding RNAs: Novel Regulators of Macrophage Homeostasis in Ocular Vascular Diseases.Biomolecules · 2024Review
- Identification of long non-coding RNA and circular RNA associated networks in cellular stress responses.Frontiers in genetics · 2023Article
- Krüppel-like factors in tumors: Key regulators and therapeutic avenues.Frontiers in oncology · 2023Review
- KLF6 facilitates differentiation of odontoblasts through modulating the expression of P21 in vitro.International journal of oral science · 2022Article
- circ-EIF6 encodes EIF6-224aa to promote TNBC progression via stabilizing MYH9 and activating the Wnt/beta-catenin pathway.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Functional analysis of the short splicing variant encoded by CHI3L1/YKL-40 in glioblastoma.Frontiers in oncology · 2022Article
- miR-373-3p Regulates the Proliferative and Migratory Properties of Human HTR8 Cells via SLC38A1 Modulation.Disease markers · 2022Article
- Mechanisms of non-coding RNA-modulated alternative splicing in cancer.RNA biology · 2022Review
- Super-enhancer-driven lncRNA-DAW promotes liver cancer cell proliferation through activation of Wnt/β-catenin pathway.Molecular therapy. Nucleic acids · 2021Article
- miR-1301-3p Promotes Cell Proliferation and Facilitates Cell Cycle ProgressionFrontiers in oncology · 2021Article
- Aberrant Expression of miR-1301 in Human Cancer.Frontiers in oncology · 2021Review
- Aberrant alternative splicing in breast cancer.Journal of molecular cell biology · 2019Review
- Translation of the circular RNA circβ-catenin promotes liver cancer cell growth through activation of the Wnt pathway.Genome biology · 2019Article
- miR-328-3p mediates the anti-tumor effect in osteosarcoma via directly targeting MMP-16.Cancer cell international · 2019Article
- Krüppel like factor 6 splice variant 1 (KLF6-SV1) overexpression recruits macrophages to participate in lung cancer metastasis by up-regulating TWIST1.Cancer biology & therapy · 2019Article
- The KLF6 splice variant KLF6-SV1 promotes proliferation and invasion of non-small cell lung cancer by up-regultating PI3K-AKT signaling pathway.Journal of Cancer · 2019Article
- Aberrant expression of alternative isoforms of transcription factors in hepatocellular carcinoma.World journal of hepatology · 2018Review
- Linc-ROR Promotes Osteogenic Differentiation of Mesenchymal Stem Cells by Functioning as a Competing Endogenous RNA for miR-138 and miR-145.Molecular therapy. Nucleic acids · 2018Article
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Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Krüppel like factor 6 (KLF6) gene encodes multiple protein isoforms derived from alternative mRNA splicing, most of which are intimately involved in hepatocarcinogenesis and tumor progression. Recent bioinformatics analysis shows that alternative mRNA splicing of the KLF6 gene produces around 16 alternatively spliced variants with divergent or even opposing functions. Intriguingly, the full-length KLF6 (KLF6-FL) is a tumor suppressor gene frequently inactivated in liver cancer, whereas KLF6 splice variant 1 (KLF6-SV1) is an oncogenic isoform with antagonistic function against KLF6-FL. Compelling evidence indicates that miRNA, the small endogenous non-coding RNA (ncRNA), acts as a vital player in modulating a variety of cellular biological processes through targeting different mRNA regions of protein-coding genes. To identify the potential miRNAs specifically targeting KLF6-FL, we utilized bioinformatics analysis in combination with the luciferase reporter assays and screened out two miRNAs, namely miR-210 and miR-1301, specifically targeted the tumor suppressive KLF6-FL rather than the oncogenic KLF6-SV1. Our in vitro experiments demonstrated that stable expression of KLF6-FL inhibited cell proliferation, migration and angiogenesis while overexpression of miR-1301 promoted cell migration and angiogenesis. Further experiments demonstrated that miR-1301 was highly expressed in liver cancer cell lines as well as clinical specimens and we also identified the potential methylation and histone acetylation for miR-1301 gene. To sum up, our findings unveiled a novel molecular mechanism that specific miRNAs promoted tumorigenesis by targeting the tumor suppressive isoform KLF6-FL rather than its oncogenic isoform KLF6-SV1.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.