Rapamycin induces autophagy and apoptosis in Kaposiform hemangioendothelioma primary cells in vitro

Topic overview

In vitro study demonstrates rapamycin's mechanism of action against Kaposiform hemangioendothelioma cells, showing dose-dependent growth inhibition through mTOR pathway blockade, induction of autophagy, and apoptosis. Findings provide molecular basis for rapamycin use in treating KHE with Kasabach-Merritt phenomenon.

Key takeaways

Rapamycin inhibits KHE cell proliferation in a dose- and time-dependent manner by arresting cell cycle in G0/G1 phase.
Rapamycin induces both autophagy (elevated LC3-II/I) and apoptosis in KHE primary cells in vitro.
Rapamycin blocks mTOR signaling pathway by reducing p-mTOR, p-S6K1, and p-4E-BP1 phosphorylation in KHE cells.
Study provides mechanistic evidence supporting rapamycin use for KHE with Kasabach-Merritt phenomenon.

Keywords

Kaposiform Hemangioendothelioma Rapamycin Mtor Pathway Autophagy Kasabach-merritt Phenomenon Vascular Tumors Pediatric Oncology

Hashtags

#VascularTumors #PediatricOncology #RapamycinTherapy #KaposiformHemangioendothelioma

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