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Long non-coding RNA HOTAIR induces the PI3K/AKT/mTOR signaling pathway in breast cancer cells

Mona Sadeghalvad1,2, Kamran Mansouri3, Hamid-Reza Mohammadi-Motlagh3

  • 1Tehran University of Medical Sciences, School of Medicine, Department of Immunology - Tehran, Iran.

Revista Da Associacao Medica Brasileira (1992)
|June 1, 2022
PubMed
Abstract

Insights

Silencing HOX antisense intergenic RNA in breast cancer cells reduced PI3K, AKT, and mTOR expression. This HOX RNA knockdown also significantly inhibited breast cancer cell proliferation, suggesting its role in cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The phosphoinositide 3-kinase/protein kinase AKT/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway is crucial for cellular metabolism and growth.
  • Aberrant activation of the PI3K/AKT/mTOR pathway is implicated in breast cancer progression and metastasis.
  • Long non-coding RNAs (lncRNAs) can modulate cell signaling pathways, and abnormal HOX antisense intergenic RNA (HOTAIR) expression is linked to breast cancer development and metastasis.

Purpose of the Study:

  • To investigate the association between the lncRNA HOX antisense intergenic RNA (HOTAIR) and the PI3K/AKT/mTOR signaling pathway in breast cancer cells.
  • To determine if HOTAIR influences the expression of key components of the PI3K/AKT/mTOR pathway.
  • To assess the impact of HOTAIR modulation on breast cancer cell proliferation.

Main Methods:

  • HOX antisense intergenic RNA (HOTAIR) was silenced in MCF-7 breast cancer cells using small interfering RNAs (siRNAs).
  • Gene expression levels of HOTAIR, PI3K, AKT, and mTOR were quantified using real-time RT-PCR.
  • Cell proliferation was analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay.

Main Results:

  • Knockdown of HOTAIR led to a significant downregulation of PI3K, AKT, and mTOR gene expression in MCF-7 cells compared to controls.
  • Silencing HOTAIR markedly reduced the proliferation rate of breast cancer cells.
  • These findings suggest a positive correlation between HOTAIR expression and PI3K/AKT/mTOR pathway activity.

Conclusions:

  • HOX antisense intergenic RNA (HOTAIR) may play a role in upregulating the PI3K/AKT/mTOR signaling pathway in breast cancer.
  • HOTAIR could contribute to breast cancer cell proliferation through its influence on this pathway.
  • Targeting HOTAIR presents a potential therapeutic strategy for breast cancer by modulating the PI3K/AKT/mTOR pathway.

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