PtdIns(3,4,5)P3-dependent Rac exchanger 1 (P-Rex1) promotes mammary tumor initiation and metastasis | Zendy

Nuthasuda Srijakotre | Zendy; Heng-Jia Liu | Zendy; Max Nobis | Zendy; Joey Man | Zendy; Hon Yan Kelvin Yip | Zendy; Antonella Papa | Zendy; Helen E. Abud | Zendy; Kurt I. Anderson | Zendy; Heidi C. E. Welch | Zendy; Tony Tiganis | Zendy; Paul Timpson | Zendy; Catriona McLean | Zendy; Lisa M. Ooms | Zendy; Christina A. Mitchell | Zendy

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PtdIns(3,4,5)P₃-dependent Rac exchanger 1 (P-Rex1) promotes mammary tumor initiation and metastasis

Author(s) -

Nuthasuda Srijakotre,

Heng-Jia Liu,

Max Nobis,

Joey Man,

Hon Yan Kelvin Yip,

Antonella Papa,

Helen E. Abud,

Kurt I. Anderson,

Heidi C. E. Welch,

Tony Tiganis,

Paul Timpson,

Catriona McLean,

Lisa M. Ooms,

Christina A. Mitchell

Publication year - 2020

Publication title -

proceedings of the national academy of sciences

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.011

H-Index - 771

eISSN - 1091-6490

pISSN - 0027-8424

DOI - 10.1073/pnas.2006445117

Subject(s) - rac1 , guanine nucleotide exchange factor , cancer research , metastasis , mammary tumor , biology , breast cancer , oncogene , cancer , rex1 , signal transduction , medicine , embryonic stem cell , microbiology and biotechnology , cell cycle , genetics , induced pluripotent stem cell , gene

Significance Breast cancer is the most common cancer in women and metastasis remains the leading cause of death. P-Rex1, a guanine nucleotide exchange factor, positively regulates Rac1-mediated oncogenic signaling. P-Rex1 is overexpressed in a subset of human breast cancers; however, little is known of its function in vivo. Here we show P-Rex1 regulates Rac1 activation in vivo in the mammary gland. Increased P-Rex1 expression enhances mammary epithelial cell proliferation and is causally associated with tumor initiation. In murine models, P-Rex1 cooperates with the neu oncogene to increase mammary tumor incidence and metastasis but not primary tumor growth. Our studies suggest that inhibiting the P-Rex1–Rac1 signaling axis may be an adjunct therapy for treating invasive cancers which exhibit increased P-Rex1 expression.

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