Fig. 6 | Signal Transduction and Targeted Therapy

Fig. 6

From: Single-cell transcriptomic profiling unravels the adenoma-initiation role of protein tyrosine kinases during colorectal tumorigenesis

Fig. 6The alternative text for this image may have been generated using AI.

Activation of JAK-STAT pathway via BMX and HCK upregulation promotes adenoma initiation. a Clonogenic assays of NCM460 cells engineered to express HCK, BMX, MATK-A, MATK-B, or their vector control. b Quantification of a. c Representative bright-field and GFP expression images of organoids at day 5 after engineering to express BMX, HCK, or vector. Scale bar, 200 μm. d Time course culture of organoids expressing BMX, HCK, or vector. Scale bar, 200 μm. e Quantification of number and size of organoids at day 16 after engineering to express BMX, HCK, or vector. f Representative bright-field (up) and H&E staining (below) images of organoids engineered to express HCK, BMX, or vector. Scale bar, 100 μm. g Co-immunofluorescence staining of E-cadherin with Ki67 was conducted for organoids engineered to express HCK, BMX, or vector. Scale bar, 100 μm. h NCM460 cells were engineered to express BMX, HCK, MATK-A, MATK-B, or vector. Cell lysates were made for immunoblot analysis with indicated antibodies. ACTIN was used as a loading control. i Effects of STAT3 knockdown on cell proliferation in vector-, BMX-, or HCK- overexpressing NCM460 cells. j Quantification of i. k BMX or HCK interacted with STAT3 directly. NCM460 cells were infected with vector-, BMX-, or HCK- overexpressing plasmid. The cell lysates were immunoprecipitated with an anti-FLAG antibody, then the precipitates and cell lysates were analyzed using western blotting with the indicated antibodies. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; analyzed using ANOVA

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