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Genes regulated by JNK signaling in MDA231-LM2 breast cancer cells

ABSTRACT: In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy. We used Affymetrix microarrays to analyze the transcriptomic output modulated by JNK activity in a lung metastatic derivative of the MDA-MB-231 breast cancer cell line, MDA231-LM2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE98237 | GEO | 2018/08/26

REPOSITORIES: GEO

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Homo sapiens

Project description:Genes regulated by JNK signaling in MDA231-LM2 breast cancer cells

| PRJNA384365 | ENA