Fig 2: Reverse transcription-quantitative PCR analysis of UBE2T expression in 30 paired gallbladder cancer tissues and adjacent noncancerous tissues. β-actin was used as the internal control. ****P<0.0001. UBE2T, ubiquitin conjugating enzyme E2T.

Fig 3: UBE2T was upregulated and associated with poor prognosis in patients with gallbladder cancer. (A) Representative hematoxylin and eosin staining images and (B) immunohistochemistry analysis of UBE2T expression in gallbladder cancer tissues and adjacent noncancerous tissues (magnification, ×200). (C) Kaplan-Meier overall survival curves for 127 patients with gallbladder cancer, stratified by high and low UBE2T expression levels. UBE2T, ubiquitin conjugating enzyme E2T.

Fig 4: Western blot analysis of UBE2T expression in 12 pairs of gallbladder cancer tissues and adjacent noncancerous tissues. β-actin was used as the internal control. UBE2T, ubiquitin conjugating enzyme E2T; N, normal tissues; C, cancer tissues.

Fig 5: ERK activation reverses the tumour‐suppressive effect of BA in cisplatin‐treated xenografts. (A) Representative images of xenograft tumours and quantitative analysis of tumour volumes in four groups: Control (NC), cisplatin (CDDP), BA + CDDP, and BA + CDDP + ERK agonist (ERKA). BA + CDDP treatment markedly reduces tumour growth compared with CDDP alone, while ERK activation restores tumour size to near‐control levels. Data are shown as mean ± SEM; *p < 0.05 vs. NC, #p < 0.05 vs. CDDP, †p < 0.05 vs. BA + CDDP. (B) Western blot analysis of xenograft lysates showing decreased UBE2T as well as monoubiquitination of FANCI and FANCD2 in the BA + CDDP group, along with suppressed ERK1/2 phosphorylation; ERK agonist treatment restores p‐ERK1/2 and UBE2T expression. β‐Actin served as the loading control for total protein. (C, D) Immunohistochemical staining of xenograft tumour sections confirming reduced UBE2T (C) and p‐ERK1/2 (D) expression in the BA + CDDP group, with re‐elevation following ERK agonist co‐treatment. Scale bar = 20 μm.