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LATS1 and LATS2 suppress breast cancer progression by maintaining cell identity and metabolic state

Noa Furth1, Ioannis S Pateras2, Ron Rotkopf3

  • 1Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.

Life Science Alliance
|November 21, 2018
PubMed

Insights

Large Tumor Suppressor (LATS) paralogs LATS1 and LATS2 have distinct roles in breast cancer. Loss of LATS2 alters metabolism, while LATS1 loss increases cancer cell plasticity and hormone therapy resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Large Tumor Suppressor (LATS) proteins are critical for maintaining cellular and tissue homeostasis.
  • Deregulated LATS activity is implicated in various cancers, including breast cancer.
  • LATS1 and LATS2 are closely related paralogs with potentially distinct functions.

Purpose of the Study:

  • To investigate the specific roles of LATS1 and LATS2 down-regulation in breast cancer.
  • To understand the distinct molecular and cellular consequences of losing either LATS1 or LATS2 in breast cancer.
  • To explore potential therapeutic vulnerabilities associated with LATS paralog loss.

Main Methods:

  • Analysis of LATS1 and LATS2 expression in human breast cancer samples.
  • Utilizing mouse models to study the impact of LATS1 or LATS2 depletion on mammary tumorigenesis.
  • Investigating metabolic changes, signaling pathway alterations (e.g., PPARγ), and cellular plasticity upon LATS paralog loss.
  • Assessing response to hormone therapy in LATS-depleted breast cancer models.

Main Results:

  • Both LATS1 and LATS2 expression are significantly down-regulated in human breast cancer.
  • Loss of either LATS1 or LATS2 accelerates mammary tumor development in mice.
  • LATS2 depletion in luminal B tumors leads to metabolic rewiring (increased glycolysis, reduced PPARγ signaling) and sensitivity to PPARγ activation.
  • LATS1 depletion promotes cancer cell plasticity, basal-like features, and resistance to hormone therapy in luminal B tumors.

Conclusions:

  • LATS1 and LATS2 play distinct, non-redundant roles in suppressing breast cancer.
  • Loss of LATS2 impacts tumor metabolism and offers a potential therapeutic target via PPARγ.
  • Loss of LATS1 contributes to tumor dedifferentiation and endocrine therapy resistance.
  • Understanding the differential roles of LATS paralogs is crucial for developing targeted breast cancer therapies.

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