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. 2019 Oct 21;48:289–300. doi: 10.1016/j.ebiom.2019.10.003

Fig. 5.

Fig 5

NIPBL loss attenuates the therapeutic responses of RTX in vitro and in vivo. (a) The sensitivity of multiple gastrointestinal cancer cell lines to RTX after NIPBL knockdown. The knockdown effects were shown in the bottom. (b) The cell viability of NUGC3 cells to MTX and PTX was determined after NIPBL knockdown. (c) RTX significantly inhibited the tumour growth of NUGC3 tumour xenografts in nude mice compared with vehicle, but failed to inhibit the tumour growth of NUGC3 tumour xenografts in vivo when NIPBL was knockdown using a doxycycline-inducible shRNA. Vehicle group, n = 9; RTX group, n = 9. The knockdown effect of NIPBL in tumour xenografts was shown in right panel. (d) RTX effectively reduced the tumour growth of HCT116 tumour xenografts in nude mice, but failed to inhibit NIPBL-knockout HCT116 tumours in vivo. The knockout effect of NIPBL in tumour xenografts was shown in the right panel. (e) RTX failed to inhibit the growth of NIPBLp.K603fs-mutated RKO and NCC-59 tumour xenografts in vivo. The expression of NIPBL, MYC and TYMS in tumour xenografts were shown in the right panel. (f-g) RTX significantly reduced the tumour growth of NIPBL-knockout HCT116 tumour xenografts with exogenously expressed MYC (f) or TYMS (g) compared with vehicle. The protein expression levels of MYC and TYMS were shown in the right panel. (h-i) After exogenously expressed with MYC (h) or TYMS (i), RTX significantly inhibited the tumour growth of NIPBLp.K603fs mutated RKO tumour xenografts with exogenously expressed MYC or TYMS compared with vehicle. The protein expression levels of MYC and TYMS were shown in right panel. Data are shown as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, p value was calculated by two-tailed Student's t-test.