ArticleInternational journal of clinical and experimental pathology2019
Long non-coding RNA CASC9 knockdown inhibits the progression of nasopharyngeal carcinoma by regulating miR-145.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Long Non-Coding RNA Cancer Susceptibility Candidate 9 Regulates the Malignant Biological Behavior of Nasopharyngeal Carcinoma Cells by Targeting miR-497-5p/Wnt3a/β-catenin Signaling Pathway.Frontiers in oncology · 2022Article
- LncRNACASC9 promotes proliferation, metastasis, and cell cycle inovarian carcinoma cells through cyclinG1/TP53/MMP7 signaling.Bioengineered · 2021Article
- Tanshinone II A enhances pyroptosis and represses cell proliferation of HeLa cells by regulating miR-145/GSDMD signaling pathway.Bioscience reports · 2020Article
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
backgroundLong non-coding RNAs (lncRNAs) have been widely confirmed to modulate many tumorigeneses, including NPC. However, the exact roles of cancer susceptibility candidate 9 (CASC9) in nasopharyngeal carcinoma (NPC) and its underlying mechanisms have not been fully established.
methodsqRT-PCR was used to determine CASC9 and miR-145 expressions. Cell apoptosis, migration, and invasion were determined by flow cytometry and transwell assays, respectively. The protein expressions of BAX, Bcl-2, MMP 9, and MMP 2 were measured by western blot. The possible binding sites between miR-145 and CASC9 were predicted by the starBase v2.0 online database and verified by a luciferase report and an RNA immunoprecipitation (RIP) assay. A xenograft tumor model was established to confirm the effects of CASC9 in NPC progression
resultsThe expression level of CASC9 was upregulated in NPC tissues and cells. The knockdown of CASC9 evidently suppressed migration and invasion but promoted apoptosis in NPC cells. In addition, the inhibition of CASC9 evidently increased the BAX protein level and inhibited the expression of the Bcl-2, MMP 9, and MPP2 proteins in NPC cells. Moreover, miR-145 was directly bound to CASC9, and its inhibition reversed the inhibitory effect of CASC9 knockdown on the progression of NPC. Furthermore, the expression of miR-145 was decreased and negatively associated with CASC9 in NPC tissues and cells. Also, the knockdown of CASC9 inhibited tumor growth
conclusionCASC9 knockdown inhibited cell migration and invasion but increased cell apoptosis in NPC cells by regulating miR-145, providing a novel insight for the treatment of NPC.
Indexed as
Identifiers
31933798PMC6949778W3009001225What 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.