Correction to: Oncogene (2016) 35, 4179–4187; doi:10.1038/onc.2015.483; published online 11 January 2016 Since the online publication of this article, the authors would like to add a new co-author, Jordyn Walter. The institutional affiliation for Jordyn Walter is: Department of Biomedical Sciences, University of Minnesota Medical School, Duluth, MN, USA

Kcnq1, which encodes for the pore-forming α-subunit of a voltage-gated potassium channel, was identified as a gastrointestinal (GI) tract cancer susceptibility gene in multiple Sleeping Beauty DNA transposon-based forward genetic screens in mice. To confirm that Kcnq1 has a functional role in GI tract cancer, we created Apc(Min) mice that carried a targeted deletion mutation in Kcnq1. Results demonstrated that Kcnq1 is a tumor suppressor gene as Kcnq1 mutant mice developed significantly more intestinal tumors, especially in the proximal small intestine and colon, and some of these tumors progressed to become aggressive adenocarcinomas. Gross tissue abnormalities were also observed in the rectum, pancreas and stomach. Colon organoid formation was significantly increased in organoids created from Kcnq1 mutant mice compared with wild-type littermate controls, suggesting a role for Kcnq1 in the regulation of the intestinal crypt stem cell compartment. To identify gene expression changes due to loss of Kcnq1, we carried out microarray studies in the colon and proximal small intestine. We identified altered genes involved in innate immune responses, goblet and Paneth cell function, ion channels, intestinal stem cells, epidermal growth factor receptor and other growth regulatory signaling pathways. We also found genes implicated in inflammation and in cellular detoxification. Pathway analysis using Ingenuity Pathway Analysis and Gene Set Enrichment Analysis confirmed the importance of these gene clusters and further identified significant overlap with genes regulated by MUC2 and CFTR, two important regulators of intestinal homeostasis. To investigate the role of KCNQ1 in human colorectal cancer (CRC), we measured protein levels of KCNQ1 by immunohistochemistry in tissue microarrays containing samples from CRC patients with liver metastases who had undergone hepatic resection. Results showed that low expression of KCNQ1 expression was significantly associated with poor overall survival.

Poly (ADP‐ribose) Polymerase (PARP) functions in gene regulation, DNA repair, and mitosis and meiosis regulation. ApcMin mice was created to have either wild type Parp1 (+/+) gene or carried a germ line knockout Parp1 (−/−) gene. Deficiency for Parp1 significantly enhanced tumorigenesis in ApcMin mice. The genes, Nf‐kappa B, Brac, Sox, Mappk, and Ctnnb, are known to be involved in DNA repair, inflammation and gene regulation, and Parp1 regulation in other tissues. We want to understand the potential mechanisms underlying Parp1's function as a tumor suppressor by measuring the changes in gene expression in Parp1 knockout (KO) colons.Colons from age and gender matched mouse pairs were used for RNA isolation. RNA was isolated using the Qiagen Rneasy Mini Kit. cDNA was created by reverse transcription (RT). Primers were designed using resources at NCBI and Primer Bank, and the specificity of PCR amplicons verified by polymerase chain reaction and gel electrophoresis. Quantitative real‐time PCR (qtRT‐PCR) was then performed to measure changes in gene expression in Parp1 KO colons compared with Parp1 wild type colons. Preliminary results indicate the loss of Parp1 modulates expression of Brca, Mappk, and Nf‐kappa B. Confirmation of these data is ongoing, along with analysis of additional candidate Parp1 target genes.