LncRNA C9orf139 can regulate the progression of esophageal squamous carcinoma by mediating the miR-661/HDAC11 axis
•LncRNA C9orf139 was highly expressed in ESCC.•LncRNA C9orf139 could negatively regulate miR-661 expression.•HDAC11 expression was negatively regulated by miR-661.•LncRNA C9orf139 regulates the progression of ESCC through the miR-661/HDAC11 axis. Increasing evidence has indicated that long non-codin...
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Published in | Translational oncology Vol. 24; p. 101487 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Inc
01.10.2022
Neoplasia Press Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | •LncRNA C9orf139 was highly expressed in ESCC.•LncRNA C9orf139 could negatively regulate miR-661 expression.•HDAC11 expression was negatively regulated by miR-661.•LncRNA C9orf139 regulates the progression of ESCC through the miR-661/HDAC11 axis.
Increasing evidence has indicated that long non-coding RNAs (LncRNAs) play multiple functions in the development of cancer and function as indicators of diagnosis and prognosis. This aim of this study was to investigate the roles LncRNA C9orF139 had in the progression of esophageal squamous carcinoma (ESCC). We found C9orf139 was highly expressed in ESCC and knock down the expression of C9orf139 significantly suppressed cell proliferation, promoted apoptosis, and inhibited migration and invasion. C9orf139 was able to negatively regulate miR-661 expression. At the same time, HDAC11 expression was negatively regulated by miR-661. The C9orf139/miR-661/HDAC11 axis was further involved in regulating the expression of the NF-κB signaling pathway. The association between the C9orf139 knockdown and the reduced tumor growth and size was observed during in vivo study. C9orf139 is highly expressed in ESCC, and is thus qualified to be used as a potential diagnostic and prognostic marker for ESCC. Its promotion of ESCC progression is achieved by mediating the miR-661/HDAC11 axis. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 1936-5233 1936-5233 |
DOI: | 10.1016/j.tranon.2022.101487 |