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Tytuł pozycji:

Up-Regulation of circEIF6 Contributes to Pancreatic Cancer Development Through Targeting miR-557/SLC7A11/PI3K/AKT Signaling

Tytuł :
Up-Regulation of circEIF6 Contributes to Pancreatic Cancer Development Through Targeting miR-557/SLC7A11/PI3K/AKT Signaling
Autorzy :
Zhang T
Li M
Lu H
Peng T
Pokaż więcej
Temat :
pancreatic cancer
circeif6
mir-557
slc7a11
pi3k/akt signaling
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Źródło :
Cancer Management and Research, Vol Volume 13, Pp 247-258 (2021)
Wydawca :
Dove Medical Press, 2021.
Rok publikacji :
2021
Kolekcja :
LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
Typ dokumentu :
article
Opis pliku :
electronic resource
Język :
English
ISSN :
1179-1322
Relacje :
https://www.dovepress.com/up-regulation-of-circeif6-contributes-to-pancreatic-cancer-development-peer-reviewed-article-CMAR; https://doaj.org/toc/1179-1322
Dostęp URL :
https://doaj.org/article/d360abdda6884b908410f6f04939d7ab
Numer akcesji :
edsdoj.360abdda6884b908410f6f04939d7ab
Czasopismo naukowe
Tiequan Zhang, Mi Li, Haofeng Lu, Tao Peng Department of Hepatobiliary Surgery, The First People’s Hospital of Jingzhou, Jingzhou 434000, People’s Republic of ChinaCorrespondence: Tiequan ZhangDepartment of Hepatobiliary Surgery, The First People’s Hospital of Jingzhou, No. 8 Hangkong Road, Shashi District, Jingzhou, Hubei 434000, People’s Republic of ChinaTel +86-716-8115036Email ztq08250825@163.comBackground: Accruing evidences have pointed out that abnormal expression of circular RNAs (circRNAs) was closely related to the development of many malignancies. The present study intended to disclose the role of circRNA eukaryotic translation initiation factor 6 (circEIF6; hsa_circ_0060055) in pancreatic cancer progression.Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the expression of circEIF6, EIF6 messenger RNA (mRNA), microRNA-557 (miR-557) and solute carrier family 7 member 11 (SLC7A11) mRNA. Cell proliferation ability, migration and invasion abilities and apoptosis were evaluated by Cell Counting Kit 8 (CCK8) assay, transwell migration and invasion assays and flow cytometry. Western blot assay was performed for the expression determination of all proteins. The predicted interaction between miR-557 and circEIF6 or SLC7A11 was confirmed by dual-luciferase reporter assay. Xenograft tumor model was used for exploring the biological function of circEIF6 in vivo.Results: CircEIF6 abundance was aberrantly up-regulated in pancreatic tumor tissues and cell lines. Cell proliferation, migration and invasion were significantly restrained while cell apoptosis was induced with the silencing of circEIF6 in pancreatic cancer cells. CircEIF6 silencing also hampered the activation of phosphatidylinositol 3-kinase (PI3K)/AKT serine/threonine kinase (AKT) pathway. CircEIF6 bound to miR-557, and circEIF6 silencing elevated the expression of miR-557 in pancreatic cancer cells. MiR-557 knockdown partly overturned circEIF6 silencing-induced effects in pancreatic cancer cells. SLC7A11 was a target of miR-557, and miR-557 overexpression suppressed malignant potential of pancreatic cancer cells partly through reducing the expression of SLC7A11. CircEIF6 knockdown blocked xenograft tumor growth in vivo.Conclusion: CircEIF6 aggravated pancreatic cancer development through promoting cell proliferation, migration and invasion and suppressing cell apoptosis through targeting miR-557/SLC7A11/PI3K/AKT signaling.Keywords: pancreatic cancer, EIF6, miR-557, SLC7A11, PI3K/AKT signaling

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