1. Supplementary figure S1 by Shin et al.
a. Kidney renal clear cell carcinoma
100 90 80 70 60 50 40 30 20 10
High
hnRNPK
and PLK1
Low
p =7.38e-7
n = 499
High PLK1
Low PLK1
120
Month survival
Surviving (%)
b. Adrenocortical carcinoma
100 90 80 70 60 50 40 30 20 10
p = 7.042e-6
n =77
High
hnRNPK
and PLK1
Low
High PLK1
Low PLK1
120
140
Month survival
Surviving (%)
Supplementary figure S1. Kaplan-Meier survival analysis. To determine whether there was a correlation between survival rate and the expression level of hnRNPK and PLK1, Kaplan-Meier analysis of 499 patients with kidney renal clear cell carcinoma (a) and 77 patients with adrenocortical carcinoma (b) using the expression levels of hnRNPK and PLK1 was performed. P values were determined by the log-rank test.

2. Supplementary figure S2 by Shin et al.c d e
Supplementary figure S2. Validation of two different siRNAs targeting hnRNPK or PLK1. (a) To verify that hnRNPK regulate PLK1 expression, various cancer cells were transfected with siRNAs targeting coding region or 3՚UTR of hnRNP K mRNA which are represented by hnRNPK siRNA #1 and #2, respectively. The level of hnRNPK and PLK1 was determined by western blot analysis. (b-c) HeLa cells were transfected with each siRNA. After 48 h post-transfection, the levels of PLK1 and cleaved PARP were determined by western blot analysis (b). Clonogenicity of transfected cells was assessed as described in “Materials and Methods” (c). (d-e) After cells were transfected with two different PLK1-targeting siRNA, the levels of PLK1 and cleaved PARP were determined by western blot analysis (d). Clonogenicity of transfected cells was assessed as described in “Materials and Methods” (e).

3. Supplementary figure S3 by Shin et al.
Supplementary figure S3. Schematics for the structure of hnRNPK and its deletion mutants.

4. Supplementary figure S4 by Shin et al.
Supplementary figure S4. Schematics of fragments of PLK1 mRNA
for biotin pull-down assay.

5. Supplementary figure S5 by Shin et al.c
Supplementary figure S5. Competitive regulation of PLK1 by hnRNPK and miRNAs. (a) To check the effect of miR-149-3p and miR-193b-5p on PLK1 expression, various cancer cells (H322, T98G, HCT116, and HepG2) were transfected with control miRNA (Con-miR) or miRNA mimics. After 48 h post-transfection, the levels of hnRNPK and PLK1 were determined by western blot analysis. The level of GAPDH was checked as a loading control. (b-c) To investigate whether hnRNPK reversed miRNA-mediated suppression of PLK1, H322 and HCT116 cells were transfected with miRNA mimics (pre-miR-149-3p and miR-193b-5p) and a hnRNPK vector (FLAG-hnRNPK). Expression of hnRNPK and PLK1 was assessed by western blot. The level of GAPDH was checked as a loading control.

6. Supplementary figure S6 by Shin et al.
Supplementary figure S6. hnRNPK reversed the suppressive effect of miR-100-5p on PLK1 expression. (a) To check the effect of miR-100-5p on PLK1 expression, HeLa cells were transfected with control miRNA (Con-miR) or miR-100-5p mimic. After 48 h post-transfection, the levels of hnRNPK and PLK1 were determined by western blot analysis. The level of GAPDH was checked as a loading control. (b) To investigate whether hnRNPK reversed miRNA-mediated suppression of PLK1, cells were transfected with pre-miR-100-5p and a hnRNPK vector (FLAG-hnRNPK). Expression of hnRNPK and PLK1 was assessed by western blot. The level of GAPDH was checked as a loading control.