Fig. 1: Experimental design of RNA-seq on 4NQO-induced esophageal lesions in mice. | Nature Communications

Fig. 1: Experimental design of RNA-seq on 4NQO-induced esophageal lesions in mice.

From: Single-cell transcriptomic analysis in a mouse model deciphers cell transition states in the multistep development of esophageal cancer

Fig. 1

a Induction of esophageal precancerous and cancerous lesions in mice. Mice were treated with 4NQO in drinking water (100 μg/ml) for 16 weeks and then kept without 4NQO treatment for another 10 weeks (upper panel). Mice were killed before (week 0), during (week 12) and after treatment (weeks 20, 22, 24, or 26), respectively. Hematoxylin–eosin (H&E) staining and immunohistochemistry (IHC) analysis of Mki67 on esophageal epithelium slides clearly identified six different pathological lesions, i.e., normal (NOR), inflammation (INF), hyperplasia (HYP), dysplasia (DYS), carcinoma in situ (CIS), and invasive carcinoma (ICA) (lower panel). Similar staining results were observed in over three visual fields from each stage of esophageal lesions (more staining image in Supplementary Fig. 2d). Scale bar, 100 μm. b Plot of principal component analysis (PCA) of mini-bulk tissue RNA-seq on different pathological lesions indicated by different colors. M month of mouse age. c Overview of the experimental design of scRNA-seq. Pathological lesions of the esophagus were dissected and digested into single-cell suspensions for further separation using FITC-CD45 antibody via FACS (1–4). CD45+ and CD45− cells whose numbers in different lesions are shown on right panel were scRNA-sequenced, respectively.

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