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. Author manuscript; available in PMC: 2020 Dec 1.
Published in final edited form as: Clin Cancer Res. 2020 Jan 22;26(11):2711–2724. doi: 10.1158/1078-0432.CCR-18-3280

Figure 3: sGal-3 induces apoptosis specifically in tumor cells:

Figure 3:

A) Western blot showing cleaved caspase-3 (17 and 19 kDa) and PARP (89 kDa) in sGal-3 treated LN229 cells at indicated times. Cleavage was inhibited by a caspase-3 inhibitor (C3I; Ac-DEVD-CHO, 100 nM).

B) Caspase-3/7 GLO assay shows kinetics of induction of caspase-3/7 cleavage following treatment with sGal-3 in LN229 but not HFF-1 cells.

C) Crystal violet cell survival assay showing that caspase-3 and −9 inhibitors prevent sGal-3-mediated cancer cell (LN229 and LnCaP prostate) death at 72 hrs. Inhibitors: caspase-3 (C3I; Ac-DEVD-CHO; 100 nM), caspase-8 (C8I; Z-IETD-FMK; 20 μM) and caspase-9 (C9I; Z-LEHD-FMK; 20 μM). Quantification is percent of sGal-3/control CM crystal violet staining. N=2 (in triplicates). *p<0.05, **p<0.01 compared to control CM (unpaired t-test)

D) Caspase-9 GLO assay shows induction kinetics of caspase-9 cleavage following treatment with 2x sGal-3 CM in LN229, but not HFF-1 cells. (N = 2)

E) sGal3 CM reduces neurosphere formation by CD133+ glioblastoma patient derived cancer stem-like cells (GSCs) in a dose-dependent fashion. Number of neurospheres formed is expressed as percent in sGal-3/control CM groups. Scale bar: 100 μm.

F) Caspase-3/7 GLO assay shows induction kinetics of caspase-3/7 cleavage after GSC treatment with sGal-3 (600 ng/ml). Normal human neural progenitor cells (NPGs) were not affected.