AI Article Synopsis

  • - Glutamine (Gln) is crucial for the survival and growth of breast cancer cells, especially in triple-negative breast cancer (TNBC), yet research on Gln transporters in this context is limited.
  • - The study found that the Gln transporter SLC38A2 is highly expressed in breast cancer cell lines and its knockdown reduces Gln uptake, inhibits cell growth, and induces autophagy.
  • - High levels of SLC38A2 are linked to poorer survival rates in breast cancer patients, particularly those with TNBC, suggesting it could be a viable target for therapies aimed at Gln-dependent tumors.

Article Abstract

Background: Glutamine (Gln) is an abundant nutrient used by cancer cells. Breast cancers cells and particularly triple-receptor negative breast cancer (TNBC) are reported to be dependent on Gln to produce the energy required for survival and proliferation. Despite intense research on the role of the intracellular Gln pathway, few reports have focussed on Gln transporters in breast cancer and TNBC.

Methods: The role and localisation of the Gln transporter SLC38A2/SNAT2 in response to Gln deprivation or pharmacological stresses was examined in a panel of breast cancer cell lines. Subsequently, the effect of SLC38A2 knockdown in Gln-sensitive cell lines was analysed. The prognostic value of SLC38A2 in a cohort of breast cancer was determined by immunohistochemistry.

Results: SLC38A2 was identified as a strongly expressed amino acid transporter in six breast cancer cell lines. We confirmed an autophagic route of degradation for SLC38A2. SLC38A2 knockdown decreased Gln consumption, inhibited cell growth, induced autophagy and led to ROS production in a subgroup of Gln-sensitive cell lines. High expression of SLC38A2 protein was associated with poor breast cancer specific survival in a large cohort of patients (p = 0.004), particularly in TNBC (p = 0.02).

Conclusions: These results position SLC38A2 as a selective target for inhibiting growth of Gln-dependent breast cancer cell lines.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7852531PMC
http://dx.doi.org/10.1038/s41416-020-01113-yDOI Listing

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