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TGF-β/SMAD4-Regulated LncRNA-LINP1 Inhibits Epithelial-Mesenchymal Transition in Lung Cancer
Chong Zhang1,2, Yajing Hao3,4,5, Yanxiao Wang1,2
1E-institutes of Shanghai Universities, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
International Journal of Biological Sciences
|November 13, 2018
Summary
Long noncoding RNA in nonhomologous end joining pathway 1 (LINP1) suppresses lung cancer metastasis. LINP1 inhibits TGF-β-induced epithelial-mesenchymal transition (EMT), controlling cell invasion and stemness.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Lung cancer is a leading cause of cancer mortality globally.
- Epithelial-mesenchymal transition (EMT) drives cancer metastasis, migration, invasion, and stemness.
- The role of long noncoding RNAs (lncRNAs) in TGF-β-induced EMT in lung cancer remains under-investigated.
Purpose of the Study:
- To investigate the role of lncRNA in nonhomologous end joining (NHEJ) pathway 1 (LINP1) in regulating TGF-β-induced EMT in human lung cancer.
- To determine the effect of LINP1 on lung cancer cell migration, invasion, and stemness.
- To elucidate the mechanism by which LINP1 influences TGF-β signaling.
Main Methods:
- Quantitative real-time PCR to measure LINP1 transcription.
- TGF-β1 stimulation assays.
- Western blotting to assess EMT markers.
- Cell migration and invasion assays.
- Stemness assays.
Main Results:
- TGF-β1 treatment inhibited LINP1 transcription in a SMAD4-dependent manner.
- LINP1 overexpression suppressed TGF-β-induced EMT, cell migration, and invasion.
- LINP1 overexpression reduced cancer stem cell populations.
Conclusions:
- LINP1 acts as a tumor suppressor in lung cancer by inhibiting TGF-β-induced EMT.
- LINP1 represents a potential therapeutic target for mitigating lung cancer metastasis.
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