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 1. Low MUC4 expression is associated with poor survival in CRC patients. (A) A significant (p < 6.09e-09) upregulation of MUC4 in normal (N=41) and downregulation in CRC patients (N=286) was analyzed in the TCGA-COAD dataset. (B) Increased expression of MUC4 is associated with better overall and disease-free survival in CRC patients’ data sets (GSE 17536 and GSE 17537). (C) Breeding strategy for the generation of a genetically engineered mouse model for Muc4^-/- by crossing with Apc^flox/flox mice. First-generation of double knockout (Apc^-/-;Muc4^-/-) animals were further crossed with inducible colon-specific Cre (Cdx2P-Cre ER^T2) mice to get final cross (Apc^-/-;Muc4^-/-;Cdx2P-CreER^T2, AMC) and its littermate controls (Apc^-/-;Cdx2P-CreER^T2, AC). (D) PCR products of Apc and Muc4 and Cdx2-cre animals of genomic DNA. Below, induction of Cre recombination by tamoxifen administration (75 mg/kg body weight, 3x) via intraperitoneally.