Fig. 1
BBN treatment led to the primary formation of BMIBC, coinciding with a remarkable induction of SNHG1 in vivo. Concurrently, the overexpression of SNHG1 was observed to enhance tumorigenicity in nude mice. A-D BBN treatment induced protein alterations of KRT14, KRT5 and CD44 in vivo. The protein levels were quantitated and presented by IOD/area. E A heat map illustrated the high-throughput sequencing results of BBN mouse urothelium at varying stages. F Mice in the BBN-treated group were administered BBN (0.05%) treatments through their drinking water as indicated, while the negative control group was given normal drinking water. The mice were sacrificed at specific time points, and their bladders were surgically removed to collect mouse urothelium. Real-time PCR was employed to assess SNHG1 expression levels. G Human normal bladder urothelial cell line UROtsa cells were treated with 400 μM BBN for different times as indicated. The cells were then extracted for total RNA isolation with TRIzol reagent and real-time PCR was performed to determine SNHG1 expression levels. GAPDH was used as an internal control. M, indicates month. H-I Athymic nude mice were subcutaneously injected in the right axillary region with SNHG1overexpressed cells and corresponding vector scramble transfectants (5 × 106 suspended in 100 μL PBS). Six weeks’ post-injection, the mice were sacrificed, and the tumors were surgically excised and photographed (H), as well as weighed (I). An asterisk (*) denotes a significant increase compared to Vector transfectants (p < 0.05)