Journal: The Journal of Biological Chemistry
Article Title: Acquisition of Chemoresistance and Other Malignancy-related Features of Colorectal Cancer Cells Are Incremented by Ribosome-inactivating Stress *
Figure Lengend Snippet: RIS exposure attenuates proapoptotic signaling molecules in vivo . A , allograft assay with CMT-93 cells pre-exposed to DON. CMT-93 C57BL/6 mouse colon cancer cells pre-exposed to 500 ng/ml DON for 24 h were dissociated into single cells with trypsin, and 5 × 10 6 cells resuspended with 200 μl of PBS were injected subcutaneously into 14-week-old male C57BL/6 mice. Seven days later, 100 mg/ml 5-FU was intraperitoneally injected, and tumors were excised surgically 24 h later. The tumor volume was calculated as tumor volume = π/6 × major diameter (W) × minor diameter (L) 2 , presented by vertical scatter plot, and statistically analyzed by unpaired two-tailed t test ( bottom panel ). The difference in tumor volume was statistically significant (**, p = 0.0022). Con , control. B , a histological section of allograft tumors was analyzed by immunohistochemistry with MIC-1, EGR-1, and ATF3. 3,3′-diaminobenzidine intensity versus hematoxylin was quantitatively assessed by HistoQuest software and statistically analyzed by unpaired two-tailed t test ( bottom panel ). **, p
Article Snippet: In contrast to our expectations, EGR-1 overexpression partly restored the levels of p53 and MIC-1, which were suppressed by RIS, although EGR-1 was definitely essential for the induction of proapoptotic molecules in response to 5-FU ( D ), implicating additional mechanisms of RIS-induced suppression of MIC-1 and p53 signals, such as translational arrest of MIC-1 and p53 by the intrinsic actions of RIS.
Techniques: In Vivo, Injection, Mouse Assay, Two Tailed Test, Immunohistochemistry, Software