Fig. 5: Gastrin promotes Golgi aggregation and cell polarization at the leading edge in PANC-1 cells through activation of the Gα12/13–RhoA–ROCK signaling pathway. | Experimental & Molecular Medicine

Fig. 5: Gastrin promotes Golgi aggregation and cell polarization at the leading edge in PANC-1 cells through activation of the Gα12/13–RhoA–ROCK signaling pathway.

From: Gastrin stimulates pancreatic cancer cell directional migration by activating the Gα12/13–RhoA–ROCK signaling pathway

Fig. 5

PANC-1 cells were allowed to grow to confluence for 24 h and were then pre-treated with Gα12 siRNA, Gα13 siRNA, Rosin, and Y27632 to inhibit expression or activity of Gα12, Gα13, RhoA, and ROCK, respectively. Cells that were scratched with tips were then stimulated with gastrin. Representative images from left to right indicate the Golgi marker protein β-cop (red), cytoskeletal F-actin (green), and cell nucleus (blue). Merged images and wind rose plots of Golgi orientation are shown. Gastrin promoted the reorganization and polarization of the Golgi apparatus at the leading edge of PANC-1 cells facing the detached line; however, a highly disorganized and fragmented Golgi apparatus was distributed in the cytoplasm. Gastrin also induced the polarization of cytoskeletal F-actin accompanied with a non-polarized morphology. Gα12 RNAi, Gα13 RNAi, Rosin, and Y27632 pre-treatment blocked the polarization of the Golgi and F-actin that was induced by gastrin. Wind rose plots indicate the Golgi orientation in cells, and only the gastrin treatment group restored proper cell polarity and Golgi orientation

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