ArticleClinical & experimental metastasis2022
miR-106a-5p carried by tumor-derived extracellular vesicles promotes the invasion and metastasis of ovarian cancer by targeting KLF6.
Article in Clinical & experimental metastasis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- The regulatory role ofOncology research · 2025Pooled it
- Tissue derived extracellular vesicles advance from disease mechanisms to clinical application.Discover nano · 2026Review
- Comparative Evaluation of HMG Family Proteins and miR-106a-5p in Low-Grade Non-Invasive and High-Grade Muscle-Invasive Papillary Urothelial Carcinoma.International journal of molecular sciences · 2026Article
- Assessment of miRNA 106a-5p and 375-3p Expression in the Context of the Wnt/β-Catenin Pathway-Comparison of Prostate Adenocarcinoma and Benign Prostatic Hyperplasia Tissues.International journal of molecular sciences · 2025Article
- LSD1 inhibition sensitizes anti-PD1 blockade immunotherapy by inhibiting the long-range attack of tumor-derived extracellular vesicles.Acta pharmaceutica Sinica. B · 2025Article
- LncRNA-MALAT1 promotes triple-negative breast cancer progression and function as ceRNA to target REEP5 by sponging miR-106a-5p.European journal of medical research · 2025Article
- Emerging roles of non-coding RNAs in modulating the PI3K/Akt pathway in cancer.Non-coding RNA research · 2025Review
- Small Extracellular Vesicles: Unraveling Their Roles in Ovarian Cancer Progression and Tapping Into Clinical Application Potential.International journal of nanomedicine · 2025Review
- AAAGUGC Seed-Containing miRNAs: Master Regulators of Cancer Pathways and Therapeutic Resistance.MicroRNA (Shariqah, United Arab Emirates) · 2025Review
- Exosomal miR-106a-5p from highly metastatic colorectal cancer cells drives liver metastasis by inducing macrophage M2 polarization in the tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2024Article
- Unraveling the extracellular vesicle network: insights into ovarian cancer metastasis and chemoresistance.Molecular cancer · 2024Review
- MiR-106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction.Animal models and experimental medicine · 2024Article
- LncRNA LINC01123 promotes malignancy of ovarian cancer by targeting hsa-miR-516b-5p/VEGFA.Genes & genomics · 2024Article
- The role of extracellular vesicles in circulating tumor cell-mediated distant metastasis.Molecular cancer · 2023Review
- Emerging Roles of Using Small Extracellular Vesicles as an Anti-Cancer Drug.International journal of molecular sciences · 2023Review
- Advances in the Biological Functions of Extracellular Vesicles and their Potential Use in Treating Oral Cancer.Cell biochemistry and biophysics · 2023Review
- Adipose Tissue-Derived Extracellular Vesicles Contribute to Phenotypic Plasticity of Prostate Cancer Cells.International journal of molecular sciences · 2023Article
- Research advances and challenges in tissue-derived extracellular vesicles.Frontiers in molecular biosciences · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-derived extracellular vesicles (EVs) promote ovarian cancer (OC) metastasis by carrying microRNAs (miRs). This study investigated the mechanism of miR-106a-5p carried by OC cell-derived EVs in OC. miR-106a-5p expression in OC tissues and cells was measured. EVs were extracted from SKOV3 cells and normal cells. The internalization of EVs in OC cells was observed. OC cells were treated with SKOV3-EVs or SKOV3-EVs overexpressing miR-106a-5p to detect the proliferation, migration, and invasion. The expression levels of miR-106a-5p, KLF6, and PTTG1 were detected and their binding relationships were identified. Combined experiments were designed to detect the effects of KLF6 and PTTG1 on OC cells. A xenograft tumor experiment was performed to verify the mechanism of EVs-miR-106a-5p and KLF6 in OC metastasis. Consequently, miR-106a-5p was enhanced in OC and correlated with OC metastasis. SKOV3-EVs promoted the proliferation, migration, and invasion of OC cells. Mechanistically, EVs carried miR-106a-5p into other OC cells, inhibited KLF6, reduced the binding of KLF6 to the PTTG1 promoter, and upregulated PTTG1 transcription. Overexpression of KLF6 or silencing of PTTG1 attenuated the promoting effect of EVs-miR-106a-5p on OC cells. EVs-miR-106a-5p facilitated OC metastasis via the KLF6/PTTG1 axis. To conclude, OC cell-derived EVs facilitated the progression and metastasis of OC via the miR-106a-5p/KLF6/PTTG1 axis.
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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.