Rapamycin induces autophagy and apoptosis in Kaposiform hemangioendothelioma primary cells in vitro | KHE primary cells from the tumor of a 1 month-old patient were isolated | Lab research | In vitro study | KHE cells were incubated in: | 4 different rapamycin concentrations and | 1 control cell line | Cells viability was assessed at: | 12 h | 24 h | 36 h | RESULTS | RAPAMYCIN | Proliferation of KHE by increasing G0/G1 phase | mTor pathway by dephosphorylation | Apoptosis & autophagy | Conclusion: | Rapamycin was cytotoxic to KHE primary cells in vitro in a dose- and time dependent manner | https://pubmed.ncbi.nlm.nih.gov/35428493/ | Source: ZuoPeng Wang et al. | Department of Pediatric Oncology, Children's Hospital of Fudan University, Shanghai, China | @StayCurrentMD | @cecilipstick | Journal of Pediatric Surgery
Rapamycin induces autophagy and apoptosis in Kaposiform hemangioendothelioma primary cells in vitro
Infographic · Sep 2022 · 1 min read
In brief
In brief
In vitro study demonstrates rapamycin's mechanism against kaposiform hemangioendothelioma by inhibiting cell proliferation, inducing apoptosis and autophagy, and blocking mTOR signaling. Findings provide molecular basis for rapamycin's clinical efficacy in treating KHE with Kasabach-Merritt phenomenon.
- Rapamycin inhibits KHE cell growth 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.
Written by the GCMD Library team from the infographic.
The infographic uses a teal and yellow color scheme with illustrated icons. The top section shows a calendar icon labeled as lab research. The middle section displays a visual representation of cell culture with a pipette and petri dishes containing stylized cells. The bottom section presents results in gray and yellow boxes with minus and plus symbols indicating inhibition and induction effects.
Background
Rapamycin has been recommended to treat Kaposiform hemangioendothelioma (KHE) with Kasabach-Merritt phenomenon (KMP), but the underlying mechanism of the clinical effect has not been established. Therefore, we determined rapamycin cytotoxicity on KHE cells in vitro and the underlying mechanism.
Methods
KHE primary cells were derived from a tumor specimen and treated with rapamycin. Immunofluorescence was applied to identify the cells. Cell viability was measured using the Cell Counting Kit-8 (CCK-8) assay. Cell cycle and apoptosis were assessed using flow cytometry (FCM). Western blots (WB) were performed to determine phosphorylation of mammalian target of rapamycin (mTOR), p70 S6 kinase (S6K1), and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1), as well light chain 3 (LC3) expression.
Results
Rapamycin inhibited the growth of KHE primary cells in a dose- and time-dependent manner. Cell cycle progression was arrested in the G0/G1 phase and apoptosis was induced. WB results showed that LC3-II/I expression was significantly elevated in KHE primary cells treated with rapamycin, while the level of p-mTOR, p-S6K1, and p-4E-BP1 expression was reduced. LC3 fluorescent spots were increased in the rapamycin treatment group.
Conclusions
Rapamycin inhibited KHE primary cell proliferation, induced apoptosis and autophagy, and blocked the mTOR signaling pathway.