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Phospho-antibody microarray analyses for wild-type and Pak1-deficient breast cancer cells

ABSTRACT: To identify differentially phosphorylated proteins between wild-type and Pak1-deficient mouse breast cancer cells, we performed a comparative study by using phospho-antibody arrays.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE192492 | GEO | 2021/12/24

REPOSITORIES: GEO

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Phospho-antibody microarray analyses for wild-type and Pak1-deficient breast cancer cells

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Project description:P21-activated kinase 1 (Pak1) is a key oncogenic kinase and a lot of work about the mechanism of Pak1 action in cancer have been reported, while it remains unknown whether Pak1 could potentially regulate the biology of regulatory miRNAs by new interacting substrate. Here, we identified that Pak1 modulated the miR-132 expression in gastric cancer cells. Pak1 interacted with and phosphorylated activating transcription factor-2 (ATF2) on Serine 62 (Ser62), which blocked ATF2 translocation into cell nucleus. We further demonstrated that ATF2 induced miR-132 transcription via binding to the miR-132 promoter in the -30 to -39 region. Moreover, overexpression of miR-132 in gastric cancer cells significantly reduced cell adhesion, migration and invasion in vitro and hematogenous metastasis in vivo. MiR-132 targeted CD44 and fibronectin (FN) and promoted lymphocytes to gather around gastric cancer cells and kill them. More importantly, downregulation of miR-132 in gastric cancer was specifically associated with hematogenous metastasis, instead of lymph node or implantation metastasis. Taken together, miR-132 is a key negative regulator in the hematogenous metastasis of gastric cancer. A novel cell signaling pathway Pak1-ATF2-miR-132-CD44/FN is established and may be a new therapeutic target for hematogenous metastasis of gastric caner.

2017-07-31 | GSE84290 | GEO

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