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LINC00092 Modulates Oxidative Stress and Glycolysis of Breast Cancer Cells via Pyruvate Carboxylase-Mediated AKT/mTOR

Wei Chen1,2, Yushan Liu1,2, Shaohong Kang1,2

  • 1Department of Breast Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian Province 350001, China.

Oxidative Medicine and Cellular Longevity
|July 8, 2022
PubMed
Abstract

Insights

Long noncoding RNA LINC00092 inhibits breast cancer progression by regulating oxidative stress and glycolysis. This occurs through the pyruvate carboxylase (PC)-mediated AKT/mTOR pathway, suggesting LINC00092 as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Noncoding RNAs (ncRNAs) represent emerging therapeutic targets in cancer treatment.
  • Breast cancer (BC) progression involves complex regulatory mechanisms including oxidative stress and glycolysis.
  • Understanding the role of specific ncRNAs like LINC00092 is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the regulatory role of LINC00092 in breast cancer (BC).
  • To explore the impact of LINC00092 on BC oxidative stress and glycolysis.
  • To elucidate the underlying molecular mechanism involving pyruvate carboxylase (PC) and the AKT/mTOR pathway.

Main Methods:

  • Bioinformatics analysis was employed to assess LINC00092 expression in BC.
  • Experimental manipulation (overexpression and silence) of LINC00092 in BC cells.
  • Assessment of BC cell proliferation, migration, invasion, oxidative stress, and glycolysis.
  • Investigation of the interaction between LINC00092 and pyruvate carboxylase (PC), and the AKT/mTOR pathway.

Main Results:

  • LINC00092 expression was found to be low in BC and inversely correlated with tumor progression.
  • Overexpression of LINC00092 suppressed BC cell proliferation, migration, invasion, oxidative stress, and glycolysis, and inhibited tumor growth *in vivo*.
  • LINC00092 directly binds to PC, modulating its ubiquitination and degradation, and influencing the AKT/mTOR pathway.

Conclusions:

  • LINC00092 plays a tumor-suppressive role in breast cancer.
  • LINC00092 regulates BC oxidative stress and glycolysis via the PC-mediated AKT/mTOR pathway.
  • LINC00092 represents a potential diagnostic and therapeutic target for breast cancer.

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