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Inhibition of ABI2 ubiquitination-dependent degradation suppresses TNBC cell growth via down-regulating PI3K/Akt

Linlin Lv1,2, Shujing Li1, Jie Kang1

  • 1School of Bioengineering & Key Laboratory of Protein Modification and Disease, Dalian University of Technology, Dalian, Liaoning Province, 116024, China.

Cancer Cell International
|June 27, 2024
PubMed

Insights

Triple negative breast cancer (TNBC) research identifies ABI2 protein as a tumor suppressor. Low ABI2 levels correlate with TNBC, and Colistimethate sodium shows potential for treating this cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Triple negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies.
  • The ubiquitin-protease system plays a role in TNBC development and progression.

Purpose of the Study:

  • To investigate the role of ABI2 protein in TNBC.
  • To identify potential therapeutic strategies targeting ABI2 for TNBC treatment.

Main Methods:

  • Bioinformatics analysis to identify ABI2.
  • Experimental validation of ABI2 expression and function in TNBC cells.
  • Molecular mechanism studies involving ubiquitination, E3 ligase CBLC, and PI3K/Akt signaling pathway.
  • Drug screening using FDA-approved compounds.

Main Results:

  • ABI2 is expressed at low levels in TNBC tumors and suppresses cell cycle, migration, invasion, and proliferation.
  • E3 ligase CBLC promotes ABI2 degradation via ubiquitination.
  • ABI2 inhibits the PI3K/Akt pathway by interacting with Rho GTPase RAC1.
  • Colistimethate sodium (CS) effectively suppresses TNBC cell proliferation and induces apoptosis.

Conclusions:

  • ABI2 functions as a tumor suppressor in TNBC by regulating cell cycle and inhibiting key signaling pathways.
  • Targeting ABI2 with compounds like Colistimethate sodium presents a promising therapeutic avenue for TNBC.
Keywords:
ABI2CBLCColistimethate sodiumPI3K/AktTNBC

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