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LRP-1 promotes cancer cell invasion by supporting ERK and inhibiting JNK signaling pathways. | LitMetric

AI Article Synopsis

  • * Researchers used silencing techniques and experiments to show that LRP-1 is a key regulator of ERK and JNK signaling pathways in tumor cells, influencing their adhesive properties and contribution to cancer invasion.
  • * The study concludes that ERK and JNK are crucial for how LRP-1 facilitates the breakdown of focal adhesions in malignant cells, supporting their invasive behavior.

Article Abstract

Background: The low-density lipoprotein receptor-related protein-1 (LRP-1) is an endocytic receptor mediating the clearance of various extracellular molecules involved in the dissemination of cancer cells. LRP-1 thus appeared as an attractive receptor for targeting the invasive behavior of malignant cells. However, recent results suggest that LRP-1 may facilitate the development and growth of cancer metastases in vivo, but the precise contribution of the receptor during cancer progression remains to be elucidated. The lack of mechanistic insights into the intracellular signaling networks downstream of LRP-1 has prevented the understanding of its contribution towards cancer.

Methodology/principal Findings: Through a short-hairpin RNA-mediated silencing approach, we identified LRP-1 as a main regulator of ERK and JNK signaling in a tumor cell context. Co-immunoprecipitation experiments revealed that LRP-1 constitutes an intracellular docking site for MAPK containing complexes. By using pharmacological agents, constitutively active and dominant-negative kinases, we demonstrated that LRP-1 maintains malignant cells in an adhesive state that is favorable for invasion by activating ERK and inhibiting JNK. We further demonstrated that the LRP-1-dependent regulation of MAPK signaling organizes the cytoskeletal architecture and mediates adhesive complex turnover in cancer cells. Moreover, we found that LRP-1 is tethered to the actin network and to focal adhesion sites and controls ERK and JNK targeting to talin-rich structures.

Conclusions: We identified ERK and JNK as the main molecular relays by which LRP-1 regulates focal adhesion disassembly of malignant cells to support invasion.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904376PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0011584PLOS

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