Fig. 4: P-STAT3 is required for S1PR1-promoted tumor growth and liver metastasis in CRC. | Cell Death & Disease

Fig. 4: P-STAT3 is required for S1PR1-promoted tumor growth and liver metastasis in CRC.

From: The mechanism of the premetastatic niche facilitating colorectal cancer liver metastasis generated from myeloid-derived suppressor cells induced by the S1PR1–STAT3 signaling pathway

Fig. 4: P-STAT3 is required for S1PR1-promoted tumor growth and liver metastasis in CRC.The alternative text for this image may have been generated using AI.

a S1PR1 and p-STAT3 protein expression levels in SW480-exS1PR1 cells transduced with lenti-shSTAT3, as revealed using Western blotting. b STAT3 knockdown significantly inhibited the growth of SW480-exS1PR1 cells, as revealed using an MTT assay. c A wound healing assay showed STAT3 knockdown significantly inhibited the migration of SW480-exS1PR1 cells, 36 h after wounding. d A transwell assay showed STAT3 knockdown significantly inhibited cell migration and invasion of SW480-exS1PR1. e The morphologic characteristics of subcutaneous tumors in STAT3 knockdown SW480-exS1PR1 cells; characteristic images of liver metastases in STAT3 knockdown SW480-exS1PR1 cells. The data shown represent the mean ± s.e.m of a representative experiment performed in triplicate (*P < 0.05, **P < 0.01)

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