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Updated: Jan 22, 2026

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
Small Nucleolar RNA 71A Promotes Lung Cancer Cell Proliferation, Migration and Invasion via MAPK/ERK Pathway
Guiliang Tang1, Zihang Zeng1, Wenjie Sun1
1Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China.
Abstract:
Objective: Increasing evidence suggested that dysregulated small nucleolar RNAs (snoRNAs) were involved in tumor development. The roles of snoRNA 71A (SNORA71A) in the progression of non-small cell lung cancer (NSCLC) remained unclear. Methods: Dataset GSE19188 from Gene Expression Omnibus (GEO) database was downloaded to detect the expression levels of SNORA71A in NSCLC tissues. The biological significance of SNORA71A was explored by loss-of-function analysis both in vitro and in vivo. Results: SNORA71A was overexpressed in NSCLC tissues compared with normal tissues, and upregulated SNORA71A was significantly associated with worse survival of NSCLC patients. Knockdown of SNORA71A suppressed proliferation of both A549 and PC9 cells, and induced G0/G1 phase arrest. Knockdown of SNORA71A also suppressed xenograft tumor growth in mice. In addition, knockdown of SNORA71A inhibited cell invasion and migration and suppressed epithelial-mesenchymal transition. Furthermore, downregulated SNORA71A decreased the phosphorylation of MEK and ERK1/2 in the MAPK/ERK signal pathway. Conclusion: SNORA71A functions as an oncogene in NSCLC and may serve as a therapeutic target and promising prognostic biomarker of NSCLC.
Insights
Small nucleolar RNA 71A (SNORA71A) is overexpressed in non-small cell lung cancer (NSCLC). SNORA71A promotes NSCLC progression and may be a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Dysregulated small nucleolar RNAs (snoRNAs) are implicated in tumor development.
- The specific role of SNORA71A in non-small cell lung cancer (NSCLC) progression was previously unclear.
Purpose of the Study:
- To investigate the expression and function of SNORA71A in NSCLC.
- To determine if SNORA71A could serve as a prognostic biomarker or therapeutic target for NSCLC.
Main Methods:
- Analysis of SNORA71A expression in NSCLC tissues using GEO dataset GSE19188.
- In vitro and in vivo loss-of-function studies (siRNA knockdown) in NSCLC cell lines and mouse xenograft models.
- Assessment of cell proliferation, cell cycle, invasion, migration, epithelial-mesenchymal transition (EMT), and MAPK/ERK signaling pathway activity.
Main Results:
- SNORA71A was significantly overexpressed in NSCLC tissues and associated with poorer patient survival.
- SNORA71A knockdown inhibited NSCLC cell proliferation, induced G0/G1 phase arrest, and suppressed tumor growth in vivo.
- Downregulation of SNORA71A reduced cell invasion, migration, EMT, and MEK/ERK phosphorylation in the MAPK/ERK pathway.
Conclusions:
- SNORA71A acts as an oncogene in NSCLC progression.
- SNORA71A represents a potential therapeutic target and a promising prognostic biomarker for NSCLC.
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