Fig. 2: CNOT7 knockdown promotes sensitivity of CRC to radiotherapy in vitro and in vivo. | Cell Death & Disease

Fig. 2: CNOT7 knockdown promotes sensitivity of CRC to radiotherapy in vitro and in vivo.

From: CNOT7 facilitates radiation resistance in colorectal cancer through TRIM21/XRCC6-mediated non-homologous end joining repair

Fig. 2: CNOT7 knockdown promotes sensitivity of CRC to radiotherapy in vitro and in vivo.

A–D CCK8 assay revealed that CNOT7 knockdown increased the radiation therapy sensitivity of CRC cells and CNOT7 overexpression promoted CRC cell resistance to radiation therapy. E, F Representative images and corresponding survival fraction curves of colony formation assays showed that CNOT7 knockdown increased radiotherapy sensitivity in HCT116. G, H Representative images and corresponding survival fraction curves of colony formation assays showed that overexpression of CNOT7 promotes radiation resistance in SW480. I, J Flow cytometry was employed to access the proportion of apoptosis in HCT116 and CNOT7 knockdown HCT116 cells with or without radiotherapy. K Flow cytometry was used to evaluate the proportion of apoptosis in SW480 and CNOT7 knockdown SW480 cells with or without radiotherapy. L Gross images of HCT116 and CNOT7 knockdown HCT116 cell-derived subcutaneous tumors with or without radiotherapy. M–O Tumor growth curves (M), tumor volume (N) and tumor weights (O) of HCT116 and CNOT7 knockdown HCT116 cell-derived subcutaneous tumors with or without radiotherapy.

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