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Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1

Z-B Zhong1, Y-J Wu, J-N Luo

  • 1Department of Head and Neck Cancer Radiation Therapy, Harbin Medical University Cancer Hospital, Harbin, China. gexiaofeng121@163.com.

European Review for Medical and Pharmacological Sciences
|December 21, 2019
PubMed
Abstract

Insights

Long non-coding RNA DLX6-AS1 promotes thyroid cancer (TC) progression. Inhibiting DLX6-AS1 suppresses TC cell migration and invasion by upregulating UPF1, suggesting DLX6-AS1 as a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Oncology
  • RNA Biology

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their critical roles in cancer development.
  • The specific involvement of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in thyroid cancer (TC) pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the role of DLX6-AS1 in thyroid cancer progression.
  • To explore the underlying molecular mechanisms by which DLX6-AS1 influences TC development.

Main Methods:

  • Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) to assess DLX6-AS1 expression in TC tissues and cells.
  • In vitro assays (Transwell, wound healing) to evaluate cell migration and invasion.
  • Western blot to analyze protein expression, including UPF1.
  • In vivo studies to confirm the functional role of DLX6-AS1 in tumor metastasis.

Main Results:

  • DLX6-AS1 expression was significantly elevated in TC tissues compared to normal tissues.
  • Knockdown of DLX6-AS1 inhibited TC cell migration and invasion in vitro.
  • DLX6-AS1 knockdown led to increased mRNA and protein expression of UPF1.
  • UPF1 expression was negatively correlated with DLX6-AS1 levels in TC tissues.
  • In vivo, DLX6-AS1 knockdown significantly suppressed tumor metastasis.

Conclusions:

  • DLX6-AS1 promotes thyroid cancer progression by enhancing cell migration and invasion.
  • The mechanism involves the downregulation of UPF1.
  • Targeting DLX6-AS1 represents a potential therapeutic strategy for thyroid cancer.

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