Fig. 6

CRs genetic interaction mediate distinct drug response and prognosis. Lung cancer cell lines with ATM mutation have worse viability when TUBA1C were knocked down in shRNA (A) and CRISPR1 (B). Cell lines with ATM mutation are sensitive to Docetaxel in CTRP (C) and GDSC1 (D). Cell lines with ATM mutation are sensitive to Vincristine in CTRP (E) and GDSC2 (F). The Kaplan–Meier overall survival of ATM mutation carriers in LUAD patients in two groups as follows: TUBA1C low-expression and TUBA1C high-expression (G). Endometrium cell lines with SETBP1 mutation have better viability when LCK were knocked down in shRNA (H) and CRISPR1 (I). Endometrium tissues with SETBP1 mutation are resistant to Dasatinib in CTRP (J) and GDSC2 (K). The Kaplan–Meier overall survival of SETBP1 mutation carriers in UCEC patients in two groups as follows: LCK low-expression and LCK high-expression (L). The cumulative effect of CSL interaction induces a better prognosis in LGG (M), UCEC (N) and SKCM (O). P values in A–F and H–K were calculated by one-sided Wilcoxon rank-sum test. P values in G, L, M, N and O were tested by log-rank test