The long noncoding RNA MIR4435-2HG enhances the migration, promotion, and glycolysis of nonsmall cell lung cancer cells by targeting the miR-371a-5p/SOX2/PI3K/Akt axis
- Jin Yang 1, Yu Su 2, Yuchen Wang 1, Kun Gao 1, Chuang Li 3, Mengmeng Li 4
- Jin Yang 1, Yu Su 2, Yuchen Wang 1
- 1Thoracic Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
- 2Department of Oncology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
- 3Operating Theatre, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
- 4Department of Pediatrics, Hebei General Hospital, Shijiazhuang, Hebei, China.
- 0Thoracic Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
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View abstract on PubMed
Summary
This summary is machine-generated.Long noncoding RNA MIR4435-2HG promotes nonsmall cell lung cancer progression by enhancing cell proliferation, migration, and glycolysis. It acts via the miR-371a-5p/SOX2 axis, offering a potential therapeutic target for this deadly cancer.
Area Of Science
- Oncology
- Molecular Biology
- RNA Biology
Background
- Nonsmall cell lung cancer (NSCLC) is a major cause of cancer mortality globally.
- The long noncoding RNA MIR4435-2HG is implicated in the carcinogenicity of various cancers.
- Understanding MIR4435-2HG's role in NSCLC is crucial for developing targeted therapies.
Purpose Of The Study
- To investigate the function of MIR4435-2HG in NSCLC.
- To elucidate the regulatory mechanism of MIR4435-2HG in NSCLC progression.
- To explore the potential of MIR4435-2HG as a therapeutic target.
Main Methods
- Quantitative real-time PCR to measure MIR4435-2HG and SOX2 expression.
- In vitro gain- and loss-of-function assays to assess cell behavior (proliferation, apoptosis, migration, invasion, glycolysis).
- In vivo nude mouse tumor model and dual-luciferase reporter assays to analyze molecular interactions.
Main Results
- MIR4435-2HG and SOX2 were upregulated in NSCLC cells.
- MIR4435-2HG overexpression increased proliferation, migration, invasion, and glycolysis while decreasing apoptosis.
- MIR4435-2HG acts as a competing endogenous RNA, targeting miR-371a-5p and upregulating SOX2, thereby promoting NSCLC progression.
Conclusions
- MIR4435-2HG drives NSCLC malignant behaviors and glycolysis through the miR-371a-5p/SOX2 pathway.
- Downregulating MIR4435-2HG exhibits antitumor effects.
- Targeting the MIR4435-2HG/miR-371a-5p/SOX2 axis represents a promising therapeutic strategy for NSCLC.
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