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Linc00152 knockdown inactivates the Akt/mTOR and Notch1 pathways to exert its anti-hemangioma effect

Yanlin Wang1, Miaomiao Li1, Changxian Dong1

  • 1Department of Hemangioma and Vascular Malformation, Henan Provincial People's Hospital, Zhengzhou 450003, China.

Life Sciences
|March 10, 2019
PubMed
Abstract

Insights

Long non-coding RNA Linc00152 promotes infantile hemangioma (IH) cell growth by activating Akt/mTOR and Notch1 pathways. Inhibiting Linc00152 reduces IH cell proliferation and induces apoptosis, offering a potential therapeutic target.

Area of Science:

  • Vascular Biology
  • Oncology
  • Molecular Biology

Background:

  • Infantile hemangioma (IH) is a common infant vascular tumor.
  • Long non-coding RNAs (lncRNAs) are implicated in oncogenesis.
  • Linc00152 is a lncRNA found to be highly expressed in IH tissues.

Purpose of the Study:

  • To investigate the oncogenic role of Linc00152 in infantile hemangioma.
  • To elucidate the underlying molecular mechanisms of Linc00152 in IH in vitro.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to measure Linc00152 expression.
  • Western blot to detect Akt/mTOR and Notch1 pathway proteins.
  • Assays for cell proliferation (Ki67, CCK-8) and apoptosis (caspase-3/7, Bcl-2, Bax).

Main Results:

  • Linc00152 expression was significantly upregulated in IH tissues and cells.
  • Linc00152 knockdown inhibited Akt/mTOR and Notch1 signaling.
  • Reduced cell proliferation and increased apoptosis were observed upon Linc00152 knockdown.
  • Overexpression of Akt or Notch1 partially reversed the effects of Linc00152 knockdown.

Conclusions:

  • Linc00152 promotes infantile hemangioma cell proliferation and inhibits apoptosis.
  • The oncogenic role of Linc00152 is mediated through the Akt/mTOR and Notch1 signaling pathways.
  • Targeting Linc00152 may represent a novel therapeutic strategy for infantile hemangioma.
Keywords:
Akt/mTORHemangioma-derived endothelial cellsInfantile hemangiomaLinc00152Long non-coding RNAsNotch1

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