Skip to main content
Fig. 6 | Experimental Hematology & Oncology

Fig. 6

From: Targeting ST8SIA6-AS1 counteracts KRASG12C inhibitor resistance through abolishing the reciprocal activation of PLK1/c-Myc signaling

Fig. 6

Targeting ST8SIA6-AS1 reverses cell resistance to KRASG12Ci in vitro. A Relative cell viability of ST8SIA6-AS1-overexpressed cells under increasing concentrations of KRASG12Ci for 72 h. B Cell colony formation of ST8SIA6-AS1-overexpressed cells treated with or without AMG510. C Western blot analysis of cells with ST8SIA6-AS1 forced expression treated by 100 nM AMG510 for 24 h. ST8SIA6-AS1-knockdown KRASG12Ci resistant cells were treated with 1 µM KRASG12Ci to determine the effect on viability by the SRB assay (72 h) (D) and colony formation assay (E). F Cell apoptosis analysis of ST8SIA6-AS1-knockdown SW1573 cells treated with or without 100 nM KRASG12Ci for 24 h. G The effect of ST8SIA6-AS1 depletion followed by 100 nM AMG510 treatment for 24 h on generating micronuclei and multi-nuclei. MIA PaCa-2-R cells were immunostained with DAPI. The percentages of abnormal mitotic cells were calculated. Scale bar 10 μm. H Immunoblotting of ST8SIA6-AS1 knockdown cells treated with 100 nM KRASG12Ci for 24 h. Statistical significance was assessed using two-tailed unpaired Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001. See also Additional file 2: Fig. S6

Back to article page