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. Author manuscript; available in PMC: 2019 Sep 6.
Published in final edited form as: Nature. 2019 Mar 6;567(7748):341–346. doi: 10.1038/s41586-019-0993-x

Extended Data Figure 6. Gboxin exerts toxicity on primary mouse GBM cells and inhibits OCR in sampled human cancer cell lines.

Extended Data Figure 6.

a. Gboxin inhibition of three primary mouse GBM cell cultures (#2396, #1661, and #1663), established from NF1/Trp53/Pten mutant GBM, treated with increasing doses of oligomycin A (oligo) or Gboxin in the presence/absence of CsA (1 μM). n = 3, mean ± SD. b-h. OCR Seahorse measurements in sampled cell lines (Colo205, A375, SK-MEL113, Cal-62, Daoy, U937, NCI-H82) under basal conditions and following addition of DMSO or Gboxin (blue or red lines respectively; 18 min.), oligomycin A (oligo; 66 min.), Fccp (84 min.), and a mixture of rotenone and antimycin A (rot/AA; 102 min.). n = 2; mean is shown. i. Viability assay for primary mouse malignant peripheral nerve sheath tumor (MPNST) cells carrying Trp53 and NF1 mutations indicates Gboxin resistance and induced sensitivity by inhibition of mPTP. Thus, Gboxin sensitivity is not directly linked to NF1 and Trp53 driver mutations. n = 3; mean ± SD.