ArticleOncology research2017
MicroRNA-98 Plays a Suppressive Role in Non-Small Cell Lung Cancer Through Inhibition of SALL4 Protein Expression.
Article in Oncology research, 2017. 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 It has been retracted, and should not be counted.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 14 papers, 1 of them a synthesis that pooled it.
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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- SALL4 and microRNA: The Role of Let-7.Genes · 2021Pooled it
- Article
- CircSFMBT2 Plays an Oncogenic Role in Lung Adenocarcinoma Depending on the miR-1305/SALL4 Axis.Biochemical genetics · 2024Article
- MicroRNA-98: the multifaceted regulator in human cancer progression and therapy.Cancer cell international · 2024Review
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- Long noncoding HOXA11-AS knockdown suppresses the progression of non-small cell lung cancer by regulating miR-3619-5p/SALL4 axis.Journal of molecular histology · 2021Article
- circRACGAP1 promotes non-small cell lung cancer proliferation by regulating miR-144-5p/CDKL1 signaling pathway.Cancer gene therapy · 2021Article
- LncRNA ST7-AS1, by regulating miR-181b-5p/KPNA4 axis, promotes the malignancy of lung adenocarcinoma.Cancer cell international · 2020Article
- microRNA-98 protects sepsis mice from cardiac dysfunction, liver and lung injury by negatively regulating HMGA2 through inhibiting NF-κB signaling pathway.Cell cycle (Georgetown, Tex.) · 2019Article
- SALL4 induces radioresistance in nasopharyngeal carcinoma via the ATM/Chk2/p53 pathway.Cancer medicine · 2019Article
- Association between quantitative parameters of CEUS and Sall4/Wnt/β-catenin signaling in patients with hepatocellular carcinoma.Cancer management and research · 2019Article
- MicroRNA-98-5p inhibits proliferation and metastasis in non-small cell lung cancer by targeting TGFBR1.International journal of oncology · 2019Article
- Curcumin Inhibits LIN-28A through the Activation of miRNA-98 in the Lung Cancer Cell Line A549.Molecules (Basel, Switzerland) · 2017Article
- Long non-coding RNA CTA sensitizes osteosarcoma cells to doxorubicin through inhibition of autophagy.Oncotarget · 2017Article
Corrections and comments
- Retraction · 2021-09-07Error in Image · Error in Results and/or Conclusions · Investigation by Third Party · Paper Mill · · see also: https://pubpeer.com/publications/3EEF82E89264CFF0A81B2C7A44F79E
- Retracted
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRs) have been demonstrated to be significantly associated with the development and progression of non-small cell lung cancer (NSCLC). However, the underlying mechanism of miR-98 in mediating the malignant phenotypes of NSCLC cells remains obscure. In this study, we found that miR-98 was significantly downregulated in NSCLC tissues compared to nontumor lung tissues. Downregulation of miR-98 was significantly associated with poor differentiation and advanced clinical stage. Restoration of miR-98 expression significantly decreased the proliferation, migration, and invasion of NSCLC A549 and H1229 cells. SALL4 was identified as a target gene of miR-98, and the protein expression of SALL4 was negatively regulated by miR-98 in NSCLC A549 and H1229 cells. Overexpression of SALL4 promoted A549 and H1229 cell proliferation, migration, and invasion and reversed the suppressive effects of miR-98 on the malignant phenotypes of A549 and H1229 cells. Moreover, SALL4 was found to be significantly upregulated in NSCLC tissues compared to the nontumor lung tissues. We then observed an inverse correlation between the miR-98 and SALL4 levels in NSCLC tissues. In vivo study revealed that miR-98 overexpression suppressed NSCLC growth. In summary, we demonstrate that miR-98 acts as a tumor suppressor in NSCLC cells by inhibiting the protein expression of its target gene SALL4. Therefore, our study highlights the importance of the miR-98/SALL4 axis in NSCLC.
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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.