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Polarity protein SCRIB interacts with SLC3A2 to regulate proliferation and tamoxifen resistance in ER+ breast cancer

Yasuhiro Saito1, Shiori Matsuda2, Naomi Ohnishi3

  • 1Institute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan. ysaito@ttck.keio.ac.jp.

Communications Biology
|May 2, 2022
PubMed

Insights

The cell polarity protein SCRIB unexpectedly promotes ER-positive breast cancer growth and endocrine resistance. SCRIB, regulated by estrogen and MYC, forms a complex with SLC3A2, impacting tamoxifen resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Estrogen receptor (ER)-positive breast cancer accounts for 75% of all cases.
  • Endocrine therapies are standard, but over 30% of patients develop resistance.
  • Understanding endocrine resistance mechanisms is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the role of the cell polarity protein SCRIB in ER-positive breast cancer.
  • To elucidate SCRIB's function in endocrine resistance.
  • To identify novel therapeutic targets for endocrine-resistant breast cancer.

Main Methods:

  • Analysis of SCRIB expression in ER-positive breast cancer cells.
  • Investigating the interaction between SCRIB, SLC3A2, and other proteins.
  • Assessing the impact of SCRIB and SLC3A2 on cell proliferation and tamoxifen resistance.

Main Results:

  • SCRIB acts as a tumor promoter and regulator of endocrine resistance in ER-positive breast cancer cells.
  • Estrogen signaling, via MYC, induces SCRIB expression.
  • SCRIB interacts with SLC3A2 to form a quaternary complex essential for amino acid transporter function.
  • SCRIB and SLC3A2 are vital for cell proliferation and tamoxifen resistance.

Conclusions:

  • SCRIB plays a significant role in promoting ER-positive breast cancer progression and endocrine resistance.
  • The SCRIB/SLC3A2 complex represents a novel therapeutic target for endocrine-resistant breast cancer.
  • Targeting this complex may overcome tamoxifen resistance in ER+ breast cancer.

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