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.

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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