LncRNA SNHG3 promoted cell proliferation, migration, and metastasis of esophageal squamous cell carcinoma via regulating miR-151a-3p/PFN2 axis

Abstract: Esophageal squamous cell carcinoma (ESCC) is an aggressive malignant tumor with a poor prognosis. The dysregulation of long non-coding RNAs (lncRNAs) is closely related to the tumorigenesis and progression of ESCC. However, the effects of lncRNA small nucleolar RNA host gene 3 (lncRNA SNHG3) in ESCC are still unclear. Therefore, a series of experiments methods, such as quantitative real-time polymerase chain reaction, function gain/loss experiments, western blots, and animal xenograft tumor model, were employed to explore the biological function and molecular mechanism of SNHG3 in ESCC. As results, we first reported that SNHG3 was significantly up-regulated in ESCC tissues and cells. SNHG3 knockdown obviously inhibited cell proliferation, migration, invasion, and promoted apoptosis. Mechanism analysis revealed that SNHG3 sponged miR-151a-3p to regulate PFN2. Inhibition of miR-151a-3p and overexpression of PFN2 attenuated the positive effect of SNHG3 knockdown on suppressing tumor progression. Furthermore, the anti-tumor effects of SNHG3 knockdown were also observed in vivo. In summary, our results indicated that SNHG3 knockdown suppressed tumor development via the miR-151a-3p/PFN2 axis, and targeting SNHG3 may provide a new opportunity for ESCC patients.

Objekt anzeigen

• Standort: Deutsche Nationalbibliothek Frankfurt am Main
• Umfang: Online-Ressource
• Sprache: Englisch

Verweise und Beziehungen

• Erschienen in: LncRNA SNHG3 promoted cell proliferation, migration, and metastasis of esophageal squamous cell carcinoma via regulating miR-151a-3p/PFN2 axis ; volume:17 ; number:1 ; year:2022 ; pages:1584-1598 ; extent:15 ; Open medicine ; 17, Heft 1 (2022), 1584-1598 (gesamt 15)

Beteiligte, Orts- und Zeitangaben

• Urheber: Ren, Tiejun ; Wang, Dingyi ; Gu, Jinjin ; Hou, Xiaozhen

Weitere Informationen

• DOI: 10.1515/med-2022-0548
• URN: urn:nbn:de:101:1-2022101514045168855586
• Rechteinformation: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.