RNA-sequencing of lung tissues from Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice at baseline and seven months post-NNK

We have shown that Gprc5a-/- mice form Kras-mutant lung tumors spontaneously which is accelerated by tobacco carcinogen (NNK) exposure. We found in these mice that Lcn2 was distinctively up-regulated along the spectrum of Kras-mutant lung cancer development. To understand the role of Lcn2 in lung cancer pathogenesis, we generated Gprc5a-/-/Lcn2-/- mice and found that these animals have increased lung tumor devleopment following NNK compared to Gprc5a-/- animals with intact Lcn2. To understand these effects, we performed RNA-sequencing (RNA-Seq) of lung tissues from Gprc5a-/-/Lcn2-/- and Gprc5a-/- mice at baseline (prior to NNK exposure) and of tumor-bearing lungs from both groups at seven months post-NNK exposure. Overall design: Groups of 9-10 of each of Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice (8 weeks old) were intraperitoneally administered 50 mg/kg body weight NNK three times per week for 8 weeks. After seven months following completion of NNK exposure, mice were sacrificed and portions of lung tissues were used for RNA isolation and subsequent RNA-Seq analysis. For comparison, lungs from 10 Gprc5a-/- and 10 Gprc5a-/-/Lcn2-/- mice (8 weeks old) were also studied at baseline (prior to NNK exposure) by RNA-Seq.