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. Author manuscript; available in PMC: 2024 Aug 1.
Published in final edited form as: Int J Cancer. 2023 May 4;153(3):552–570. doi: 10.1002/ijc.34528

Fig. 1.

Fig. 1

TGF-β decreases KMT2D expression through the upregulation of miR-147b. (A) Comparing KMT2D nascent mRNA synthesis (Bru-seq) and mRNA degradation (BruChase-seq) between vehicle control- and 72h TGF-β-treated PANC-1 cells. Exons were labeled as solid red bars and introns as white bars in between exons. (B) Western blot analysis of KMT2D protein in PANC-1 cells treated with TGF-β for 24, 48, and 72 hours compared to vehicle-treated cells. Vinculin was used as loading control. (C) Western blot analysis of KMT2D in BxPC-3 cells treated with TGF-β with or without a TGF-β inhibitor, SB505124, for 72 hours. Vinculin was used as loading control. (D) Bru-seq analysis of miR-147b transcription in PANC-1 cells treated with TGF-β for 1, 24, and 72 hours compared to vehicle-treated cells. (E) Quantitative real-time PCR of mature miR-147b in PANC-1 and BxPC-3 cells treated with DMSO or TGF-β for 48 hours with or without SB505124. U6 was used as the reference gene. (****p<0.0001, Two-way ANOVA with Dunnett’s multiple comparisons test, n=3) (F) Western Blot analysis of KMT2D in PANC-1, BxPC-3, and MIA PaCa-2 cells transfected with miR-147b mimic or miR-147b inhibitor (miR147i). β-actin was used as loading control.