ArticleComputational and mathematical methods in medicine2022
lncRNA MSC-AS1/miRNA-429 Axis Mediates Growth and Metastasis of Nasopharyngeal Carcinoma via JAK1/STAT3 Signaling Pathway.
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 It has been retracted, and should not be counted.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 2 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
2 citing papers in PubMed, 4 citations in OpenAlex.
- HIF-1-Induced hsa-miR-429: Understanding Its Direct Targets as the Key to Developing Cancer Diagnostics and Therapies.Cancers · 2023Review
- Retracted: lncRNA MSC-AS1/miRNA-429 Axis Mediates Growth and Metastasis of Nasopharyngeal Carcinoma via JAK1/STAT3 Signaling Pathway.Computational and mathematical methods in medicine · 2023Article
Corrections and comments
- Retraction · 2023-11-29Compromised Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: We attempted to clarify the effect of lncRNA MSC-AS1 on carcinogenic and development of nasopharyngeal carcinoma (NPC) and the related mechanisms. Methods: The levels of MSC-AS1 and miR-429 were estimated in NPC tissues and cells using qRT-PCR. Correlation analysis, dual-luciferase report, and RNA pull down assay assessed the action association of MSC-AS1 and miR-429. MTT, colony formation, cell wound scratch, and transwell assays were used to assess the proliferation, invasion, and migration of C666-1 cells. Metastasis-related protein expressions and activation of the JAK1/STAT3 pathway were confirmed by western blot and immunohistochemistry. Results: The expression of MSC-AS1 presented significant upregulation, and miR-429 expression was markedly downregulated in NPC tissues and cells. The level of MSC-AS1 had negative relation to the miR-429 level. Knockdown of MSC-AS1 suppressed the proliferation, invasion, and migration of C666-1 cells. On the contrary, overexpressing of MSC-AS1 exerts the opposite effects on C666-1 cell growth and migration. miR-429 was determined as functional downstream of MSC-AS1. The suppressive function of MSC-AS1 knockdown was predominately abolished by the miR-429 inhibitor. miR-429 was an antitumor gene inhibiting NPC growth and metastasis through JAK1/STAT3 pathway. In C666-1 cells, the elevated cell growth and migration induced by the miR-429 inhibitor were significantly reversed by si-JAK1 transfection. Conclusions: High expression of MSC-AS1 exerted a carcinogenic effect on NPC cell growth and metastasis by inhibiting miR-429 and activating the JAK1/STAT3 pathway.
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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.