ArticleComputational and mathematical methods in medicine2022
lncRNA NUTM2A-AS1 Targets the SRSF1/Trim37 Signaling Pathway to Promote the Proliferation and Invasion of Breast Cancer.
Article in Computational and mathematical methods in medicine, 2022. 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 It has been retracted, and should not be counted.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 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- LncRNA BBOX1-AS1 Contributes to Laryngeal Carcinoma Progression by Recruiting SRSF1 to Maintain EFNB2 mRNA Stability.Biochemical genetics · 2025Article
- The role of lncRNA binding to RNA‑binding proteins to regulate mRNA stability in cancer progression and drug resistance mechanisms (Review).Oncology reports · 2024Review
- H3K27ac-activated LncRNA NUTM2A-AS1 Facilitated the Progression of Colorectal Cancer CellsCurrent cancer drug targets · 2024Article
- Retracted: lncRNA NUTM2A-AS1 Targets the SRSF1/Trim37 Signaling Pathway to Promote the Proliferation and Invasion of Breast Cancer.Computational and mathematical methods in medicine · 2023Article
Corrections and comments
- Retraction · 2023-09-27Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Concerns/Issues about Referencing/Attributions · Concerns/Issues about Peer Review · Informed/Patient Consent - None/Withdrawn · Investigation by Journal/Publisher · Investigation by Third Party · Lack of IRB/IACUC Approval and/or Compliance · Paper Mill · Computer-Aided Content or Computer-Generated Content · Unreliable Results and/or Conclusions · · See also: https://pubpeer.com/publications/92E9F20EE1109B65338FB2952EB8A8
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Method: Using the tumor database (TCGA) and analysis platform (GEPIA), NUTM2A-AS1 expression in breast cancer cases was compared with the normal cases. In addition, Kaplan-Meier curve of overall survival according to the various levels of NUTM2A-AS1 was assessed. Then, we constructed a knockdown plasmid of NUTM2A-AS1 and successfully reduced the expression function of NUTM2A-AS1 in BC cells. Results: We found NUTM2A-AS1 could promote the malignant phenotype of proliferation and invasion of BC. In terms of mechanism research, NUTM2A-AS1 was mainly located in the cytoplasm of BC cells, which indicated that NUTM2A-AS1 may achieve its function through transcriptional or posttranscriptional regulation pathways. While knocking down NUTM2A-AS1, we detected several major molecules of the trim family. The results showed that only trim37 mRNA was significantly affected, and protein detection also showed that knockdown NUTM2A-AS1 expression could reduce the expression of trim37. The results of RIP experiments suggested that NUTM2A-AS1 played a key role by combining with SRSF1 and affecting the interaction between SRSF1 and trim37 mRNA. The stability test of mRNA also confirmed that during the knockdown of NUTM2A-AS1, the mRNA stability of trim37 decreased significantly, but this downward trend could be reversed by overexpressed SRSF1. The above results suggested that NUTM2A-AS1 could maintain the stability and expression of trim37 through SRSF1 pathway. The results of rescue experiment showed the overexpression of trim37, while knocking down NUTM2A-AS1 could reverse the decrease of proliferation and invasiveness of BC cells induced by NUTM2A-AS1 knockdown. Conclusion: Therefore, trim37 is seen as a necessary target for NUTM2A-AS1 to exert the biological function of BC. Additionally, NUTM2A-AS1 is to regulate the malignant phenotype of BC through NUTM2A-AS1/trim37 pathway.
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