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LINC00092 Enhances LPP Expression to Repress Thyroid Cancer Development via Sponging miR-542-3p

Huan Wang1

  • 1General Practice Section, Wuhan University of Science and Technology Hospital, Wuhan, China.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|November 7, 2023
PubMed

Insights

Long non-coding RNA LINC00092 restrains thyroid cancer (TC) development by regulating miR-542-3p and lipoma preferred partner (LPP). Overexpressing LINC00092 inhibits TC cell proliferation and invasion, offering a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Thyroid cancer (TC) progression is influenced by poorly understood genetic factors.
  • The role of long non-coding RNA LINC00092 in thyroid cancer tumorigenesis remains largely elusive.
  • Identifying novel regulatory mechanisms is crucial for developing effective TC treatments.

Purpose of the Study:

  • To elucidate the role of LINC00092 in thyroid cancer development.
  • To investigate the regulatory mechanism involving LINC00092, miR-542-3p, and lipoma preferred partner (LPP) in TC.
  • To assess the potential of the LINC00092/miR-542-3p/LPP axis as a therapeutic target for TC.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to assess expression levels of LINC00092, miR-542-3p, and LPP in TC tissues and cells.
  • RNA immunoprecipitation and dual-luciferase reporter assays to confirm interactions between LINC00092, miR-542-3p, and LPP.
  • Cell proliferation, invasion, and colony formation assays, alongside a murine xenograft model, to evaluate the functional impact of LINC00092 and miR-542-3p on TC in vitro and in vivo.

Main Results:

  • LINC00092 expression was significantly downregulated in TC tissues and cells, while miR-542-3p was upregulated.
  • LINC00092 overexpression suppressed TC cell proliferation, invasion, and tumor growth in vivo, acting as an antineoplastic factor.
  • miR-542-3p targeted LPP and exerted opposite functions to LINC00092, promoting TC progression; its effects were reversed by LINC00092 and attenuated by LPP.

Conclusions:

  • LINC00092 functions as an antineoplastic long non-coding RNA in thyroid cancer.
  • The study reveals a novel regulatory pathway where LINC00092 restrains TC development by modulating the miR-542-3p/LPP axis.
  • The LINC00092/miR-542-3p/LPP pathway represents a promising therapeutic target for thyroid cancer treatment.

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