Depletion of transmembrane mucin 4 (Muc4) alters intestinal homeostasis in a genetically engineered mouse model of colorectal cancer

Ramesh Pothuraju; Priya Pai; Sanjib Chaudhary; Jawed A. Siddiqui; Jesse L. Cox; Sukhwinder Kaur; Satyanarayana Rachagani; Hemant K. Roy; Michael Bouvet; Surinder K. Batra

doi:doi:10.18632/aging.203935

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Priority Research Paper Volume 14, Issue 5 pp 2025—2046

Depletion of transmembrane mucin 4 (Muc4) alters intestinal homeostasis in a genetically engineered mouse model of colorectal cancer

Figure 7. Additional Kras mutation aggravates Apc tumors and reduces survival. (A) Breeding strategy for generation of genetically engineered mice model for Muc4^-/- by crossing with Apc^flox/flox and Kras^G12D mutant mice. First-generation of Apc^-/-;Muc4^-/-;Kras^G12D/+ animals were further crossed with inducible colon specific Cre (Cdx2P-Cre ER^T2) mice to get final cross (Apc^-/-;Muc4^-/-; Kras^G12D/+;Cdx2P-CreER^T2, AKMC) and its littermate controls (Apc^-/-;Kras^G12D/+;Cdx2P-CreER^T2, AKC). (B) Representative images of the colon in AKC and AKMC animals. (C) H&E images showed a grade of dysplasia in AKC and AKMC mice. n = 3 for AKC and n=6 for AKMC group. (D) Overall survival curves of different mouse models used in the present study. ns = non-significant.