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Updated: Feb 15, 2026

Author Spotlight: A Computational Pipeline for Analyzing Chimeric Noncoding RNA-Target RNA Interactions in High-Throughput Sequencing Data
Published on: December 1, 2023
Long noncoding RNA NEAT1 regulate papillary thyroid cancer progression by modulating miR-129-5p/KLK7 expression
Hong Zhang1,2, Yuechang Cai2, Li Zheng2
1Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Guangzhou, Guangdong, China.
Abstract:
Considering the dilemma in papillary thyroid cancer treatment, this study intended to find solution in molecular respect. By probing into lncRNA-NEAT1/miR-129-5p/KLK7 interaction, this study would provide new targets for future treatment. Microarray analysis and R language package were applied to select possible lncRNA and miRNA. Luciferase reporter assay and RNA pull-down test were employed in the detection of target relationship between lncRNA and miRNA. Clone formation assay, flow cytometry analysis, wound healing assay, and transwell assay were, respectively, used to observe effects of lncRNA NEAT1/miR-129-5p/KLK7 to papillary thyroid cancer cells. Western blot and qRT-PCR were used to validate protein expressions and mRNA expressions in PTC tissues and cells. LncRNA NEAT1 was highly expressed in PTC tissues and cell lines and could deteriorate PTC by promoting proliferation, invasion, and migration accompanied by less apoptosis. Besides, miR-129-5p/lncRNA NEAT1 were found to negatively correlate with each other by direct target relationship and their combination suppressed the progression of PTC. KLK7, a highly expressed downstream protein in PTC tissues, could be directly regulated by miR-129-5p in a negative way. KLK7 accelerated the deterioration of PTC in vitro experiments which could be reversed by sh-lnc RNA NEAT1 and miR-129-5p mimics. In vivo experiments, silence of lncRNA NEAT1 restrain tumor growth in weight and volume. In conclusion, lncRNA NEAT1 suppression could inhibit PTC progression by upregulating miR-129-5p, which suppressed KLK7 expression either in vitro or vivo experiments.
Insights
Suppression of long non-coding RNA NEAT1 inhibits papillary thyroid cancer progression by upregulating miR-129-5p, which suppresses KLK7. This molecular insight offers new therapeutic targets for papillary thyroid cancer (PTC).
Area of Science:
- Molecular Oncology
- Cancer Biology
- Genetics
Background:
- Papillary thyroid cancer (PTC) presents treatment challenges.
- Identifying novel molecular targets is crucial for effective PTC therapy.
Purpose of the Study:
- To investigate the lncRNA-NEAT1/miR-129-5p/KLK7 interaction in papillary thyroid cancer.
- To explore the therapeutic potential of targeting this pathway for PTC treatment.
Main Methods:
- Microarray analysis and R language for lncRNA/miRNA selection.
- Luciferase reporter and RNA pull-down assays for target validation.
- In vitro (proliferation, apoptosis, invasion, migration) and in vivo assays to assess functional effects.
- Western blot and qRT-PCR for expression analysis.
Main Results:
- Long non-coding RNA NEAT1 (lncRNA NEAT1) is upregulated in PTC and promotes proliferation, invasion, and migration while reducing apoptosis.
- lncRNA NEAT1 and miR-129-5p negatively correlate and their combined action suppresses PTC progression.
- miR-129-5p directly targets and downregulates KLK7, a protein that accelerates PTC deterioration.
- Silencing lncRNA NEAT1 inhibits tumor growth in vitro and in vivo.
Conclusions:
- lncRNA NEAT1 suppression is a potential therapeutic strategy for PTC.
- Upregulating miR-129-5p and subsequently suppressing KLK7 expression are key mechanisms involved.
- The lncRNA-NEAT1/miR-129-5p/KLK7 axis represents a promising therapeutic target for papillary thyroid cancer.
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