ArticleAmerican journal of translational research2022
LncRNA MIR4435-2HG promotes proliferation, migration, invasion and epithelial mesenchymal transition via targeting miR-22-3p/TMEM9B in breast cancer.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Identification and Validation of Basement Membrane Related LncRNA Signatures as a Novel Prognostic Model for Hepatocellular Carcinoma.Biochemical genetics · 2025Article
- The Emerging Role of LncRNA AWPPH in Multiple Cancers: A Review Study.Current molecular medicine · 2025Review
- Review
- Biological Roles and Pathogenic Mechanisms of LncRNA MIR4435-2HG in Cancer: A Comprehensive Review.Current issues in molecular biology · 2023Review
- miR-22-enriched breast cancer cells display repressed glycolytic metabolism, increased glycogen synthesis, and reduced survival in low glucose conditions.Molecular biology reports · 2023Article
- M2 Macrophage-Derived Exosomal lncRNA MIR4435-2HG Promotes Progression of Infantile Hemangiomas by Targeting HNRNPA1.International journal of nanomedicine · 2023Article
- Long non-coding RNA MIR4435-2HG: a key molecule in progression of cancer and non-cancerous disorders.Cancer cell international · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveBreast cancer, as a malignancy with the highest incidence and mortality in women, seriously threatens women's life and health. Pieces of evidence have suggested that long non-coding RNAs (lncRNAs) possess important roles in regulating the occurrence and development of breast cancer.
methodsRT-qPCR was used to explore the expression levels of MIR4435-2HG, miR-22-3p and TMEM9B in breast cancer tissues and cell lines. Cell viability, proliferation, migration and invasion were assessed by CCK-8 assay, Colony formation assay, Wound healing assay and Transwell assay, respectively. The effect of MIR4435-2HG on EMT progress was explored by Immunofluorescence assay and Western blot. RNA pull-down analysis and Dual-luciferase reporter assay were performed to validate the interaction between MIR4435-2HG and miR-22-3p, as well as miR-22-3p and TMEM9B.
resultsMIR4435-2HG was notably up-regulated in breast cancer tissues and cell lines. Additionally, down-regulation of MIR4435-2HG restrained the viability, proliferation, migration, invasion and EMT of breast cancer cells. MiR-22-3p expression was down-regulated in breast cancer tissues and cell lines, and negatively associated with MIR4435-2HG expression. Over-expression of miR-22-3p obviously inhibited the viability, proliferation, migration, invasion and EMT of breast cancer cell lines. Furthermore, TMEM9B was up-regulated in breast cancer tissues and cell lines and negatively associated with miR-22-3p expression. TMEM9B inhibition partially restored the effects of MIR4435-2HG/miR-22-3p on the viability, proliferation, migration, invasion and EMT of breast cancer cell lines.
conclusionMIR4435-2HG plays a potential tumor-promoting role in the occurrence and development of breast cancer, possibly by regulating the miR-22-3p/TMEM9B axis.
Indexed as
Identifiers
36105009PMC9452358W4295904943What OpenQuestion holds
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.