ArticleFrontiers in cell and developmental biology2021
Extracellular Vesicles Carry lncRNA SNHG16 to Promote Metastasis of Breast Cancer Cells
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- SNHG16 promotes breast cancer progression by regulating the hsa-let-7b-5p/AURKA axis.Biochemistry and biophysics reports · 2025Article
- Non-coding RNAs, a double-edged sword in breast cancer prognosis.Cancer cell international · 2025Review
- Quantitative estimates of the regulatory influence of long non-coding RNAs on global gene expression variation using TCGA breast cancer transcriptomic data.PLoS computational biology · 2024Article
- The role of extracellular vesicles in circulating tumor cell-mediated distant metastasis.Molecular cancer · 2023Review
- The role of non-coding RNAs in extracellular vesicles in breast cancer and their diagnostic implications.Oncogene · 2023Review
- The value of urinary exosomal lncRNA SNHG16 as a diagnostic biomarker for bladder cancer.Molecular biology reports · 2023Article
- Deciphering the Functional Status of Breast Cancers through the Analysis of Their Extracellular Vesicles.International journal of molecular sciences · 2023Review
- Tumor-derived nanoseeds condition the soil for metastatic organotropism.Seminars in cancer biology · 2023Review
- Non-Coding RNAs Derived from Extracellular Vesicles Promote Pre-Metastatic Niche Formation and Tumor Distant Metastasis.Cancers · 2023Review
- Non-Coding RNAs of Extracellular Vesicles: Key Players in Organ-Specific Metastasis and Clinical Implications.Cancers · 2022Review
- Long non-coding RNAWorld journal of stem cells · 2022Article
- Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b.Investigative and clinical urology · 2022Article
- Long non-coding RNA ZFY-AS1 represses periodontitis tissue inflammation and oxidative damage via modulating microRNA-129-5p/DEAD-Box helicase 3 X-linked axis.Bioengineered · 2022Article
- Tamoxifen resistance-related ceRNA network for breast cancer.Frontiers in cell and developmental biology · 2022Article
- Novel lncRNA SNHG16 Promotes the Growth and Metastasis of Malignant Melanoma by Regulating miR-205-5p/PAK2 Axis.Clinical, cosmetic and investigational dermatology · 2022Article
Corrections and comments
- Retraction · 2024-06-14Concerns/Issues about Data · Investigation by Journal/Publisher · Objections by Author(s) · Unreliable Data ·
- Retracted
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer (BC) represents the most commonly diagnosed malignancy among women. Long non-coding RNAs (lncRNAs) can be transferred by extracellular vesicles (EVs) to participate in BC progression. This study demonstrated that SNHG16 expression was significantly increased in BC tissues and cells. Overexpression of SNHG16 promoted the migration, invasion, and epithelial-mesenchymal transition (EMT) of BC cells. SNHG16 was carried by EVs. Bioinformatics analysis predicted that SNHG16 regulated PPAPDC1A expression by sponging miR-892b, which was confirmed by RNA-fluorescence
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Registered trials
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.