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Circ_0013359 facilitates the tumorigenicity of melanoma by regulating miR-136-5p/RAB9A axis

Authors :
Qi Zhang
Jiangang Feng
Yingfa Feng
Jinming Zhang
Lili Huang
Source :
Open Life Sciences, Vol 16, Iss 1, Pp 482-494 (2021), Open Life Sciences
Publication Year :
2021
Publisher :
De Gruyter, 2021.

Abstract

Background Circular RNAs play crucial roles in tumor occurrence and progression. This research aimed to explore the role and potential mechanism of hsa_circ_0013359 (circ_0013359) in melanoma. Methods The levels of circ_0013359, microRNA-136-5p (miR-136-5p), and member RAS oncogene family (RAB9A) in melanoma tissues and cells were detected using quantitative reverse transcriptase-polymerase chain reaction or western blot. Cell proliferation, apoptosis, cell cycle, cell migration, and invasion were evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, colony formation assay, flow cytometry, and transwell assay. Glycolysis was determined by detecting glucose consumption, lactate production, and extracellular acidification rate. The levels of hexokinase 2 and lactate dehydrogenase A were examined by western blot. The targeting relationship between miR-136-5p and circ_0013359 or RAB9A was confirmed by dual-luciferase reporter assay. Xenograft experiments were used to analyze tumor growth in vivo. Results Circ_0013359 and RAB9A levels were increased, while the miR-136-5p level was reduced in melanoma tissues and cells. Circ_0013359 knockdown inhibited proliferation, migration, invasion, and glycolysis and promoted apoptosis and cycle arrest in A875 and SK-MEL-1 cells. Circ_0013359 sponged miR-136-5p to regulate melanoma progression. In addition, miR-136-5p suppressed melanoma progression by targeting RAB9A. Besides, circ_0013359 silencing inhibited tumor growth in vivo. Conclusion Depletion of circ_0013359 hindered melanoma progression by regulating miR-136-5p/RAB9A axis.

Details

Language :
English
ISSN :
23915412
Volume :
16
Issue :
1
Database :
OpenAIRE
Journal :
Open Life Sciences
Accession number :
edsair.doi.dedup.....8fbd2e43a720db0ff98bda268f7ff1a8