ArticleJournal of thoracic disease2021
Knockdown of lncRNA TUC338 inhibits esophageal cancer cells migration and invasion.
Article in Journal of thoracic disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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10 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundLong non-coding RNAs (lncRNAs) are firmly identified with the event and improvement of tumors. Therefore, elucidating the functions and mechanisms of related lncRNAs is significant for understanding the occurrence and advancement of tumors. The recently discovered lncRNA TUC338 has been shown to play the role of an oncogene in an assortment of tumors. Be that as it may, the articulation and elements of lncRNA TUC338 in esophageal cancer are as yet hazy. This investigation plans to explain the capacities and related molecular mechanisms of lncRNA TUC338 in esophageal malignancy.
methodsFirstly, the expression of TUC338 in 50 instances of esophageal disease tissues and nearby tissues was detected by fluorescence reckonable PCR, and correlations with the clinic pathological characteristics of patients was further analyzed. Then, a lentiviral interference vector was designed and transfected into an esophageal cancer cell line, and knockdown was verified by fluorescence quantitative PCR. The effects of TUC338 knockdown on the proliferation, clone formation, and migration and infringement of esophageal malignancy cells were tested utilizing the CCK-8 assay, clone formation experiments, and Transwell experiments. Western blot detected the expression of invasion-related proteins.
resultsFluorescence reckonable PCR exhibit that TUC338 was exceptionally communicated in esophageal cancer tissues, and was significantly related with metastasis and TNM stage in tolerant. Functional experiments showed that in esophageal disease cell lines, knocking down the declaration of TUC338 significantly inhibited cell multiplication, clone development, and intrusion and movement. Further experiments on molecular mechanisms showed that knocking down TUC338 inhibited statement of N-cadherin and vimentin in cells.
conclusionsTUC338 is exceptionally communicated in esophageal malignancy tissues and can regulate cell proliferation and invasion.
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