ArticleIUBMB life2015
MicroRNA-200 promotes lung cancer cell growth through FOG2-independent AKT activation.
Article in IUBMB life, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed.
- Activated protein C promotes human lung cancer progression through the release of tumor extracellular vesicles and transfer of microRNA-200a.Cell death & disease · 2025Article
- A Robust NSCLC Biomarker- miR-7-5p: ItsMicroRNA (Shariqah, United Arab Emirates) · 2025Article
- Diagnostic value of microRNA-200 expression in peripheral blood-derived extracellular vesicles in early-stage non-small cell lung cancer.Clinical and experimental medicine · 2024Article
- MicroRNA‑mediated regulation in lung adenocarcinoma: Signaling pathways and potential therapeutic implications (Review).Oncology reports · 2023Review
- MiRNAs in Lung Adenocarcinoma: Role, Diagnosis, Prognosis, and Therapy.International journal of molecular sciences · 2023Review
- Advances in the role of microRNAs associated with the PI3K/AKT signaling pathway in lung cancer.Frontiers in oncology · 2023Review
- MiRNAs in Lung Cancer: Diagnostic, Prognostic, and Therapeutic Potential.Diagnostics (Basel, Switzerland) · 2022Review
- Revisiting the miR-200 Family: A Clan of Five Siblings with Essential Roles in Development and Disease.Biomolecules · 2022Review
- miR-200a/b/-429 downregulation is a candidate biomarker of tumor radioresistance and independent of hypoxia in locally advanced cervical cancer.Molecular oncology · 2022Article
- Bioinformatics analyses and biological function of lncRNA ZFPM2-AS1 and ZFPM2 gene in hepatocellular carcinoma.Oncology letters · 2020Article
- MicroRNA-106b-5p promotes hepatocellular carcinoma development via modulating FOG2.OncoTargets and therapy · 2019Article
- Identification of dysregulated long non-coding RNAs/microRNAs/mRNAs in TNM I stage lung adenocarcinoma.Oncotarget · 2017Article
- The Functions of MicroRNA-200 Family in Ovarian Cancer: Beyond Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2017Review
- Genetic variants in regulatory regions of microRNAs are associated with lung cancer risk.Oncotarget · 2016Article
- miR-8 modulates cytoskeletal regulators to influence cell survival and epithelial organization in Drosophila wings.Developmental biology · 2016Article
- [Advanced Research on MicroRNAs and EGFR-TKIs Secondary Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
MicroRNA-200 (miR-200) has emerged as a regulator of the PI3K/AKT pathway and cancer cell growth. It was reported that miR-200 can activate PI3K/AKT by targeting FOG2 (friend of GATA 2), which directly binds to the p85α regulatory subunit of PI3K. We found that miR-200 was elevated in early stage lung adenocarcinomas when compared with normal lung tissues, and the expression of miR-200 promoted the tumor spheroid growth of lung adenocarcinoma cells. We show that AKT activation was essential for such oncogenic action of miR-200. However, depletion of FOG2 had little effect on AKT activation. By performing a reverse-phase protein array, we found that miR-200 not only activated AKT but also concomitantly inactivated S6K and increased IRS-1, an S6K substrate that is increased on S6K inactivation. Depletion of IRS-1 partially inhibited the miR-200-dependent AKT activation. Taken together, our results suggest that miR-200 may activate AKT in lung adenocarcinoma cells through a FOG2-independent mechanism involving IRS-1. Our findings also provide evidence that increased miR-200 expression may contribute to early lung tumorigenesis and that AKT inhibitors may be useful for the treatment of miR-200-dependent tumor cell growth.
Indexed as
Identifiers
What 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.