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. 2022 May 21;8:48. doi: 10.1038/s41421-022-00395-1

Fig. 6. TM9SF1 depletion reverses PCIF1 knockdown-induced phenotypes.

Fig. 6

a Western blot analysis of TM9SF1 in BGC-823 cells infected with the indicated lentivirus-based shRNAs. b, c Migration analysis of BGC-823 cells with the indicated lentivirus-based shRNAs. Representative images of invaded cells are shown (b). The invaded cells were quantified (c). Scale bars, 100 μm. df BGC-823 cells with the indicated lentivirus-based shRNAs were intravenously injected into SCID mice, respectively. Representative images of gross lungs and H&E-stained lung are shown (d). The lung weight (e) and the number of metastatic nodules (>1 mm) (f) were quantified. Scale bars, 1 cm. g The working model of PCIF1-dependent m6Am modification of TM9SF1 mRNA to promote gastric cancer progression. When PCIF1 level is high, it modifies TM9SF1 mRNA with m6Am leading to decreased translational efficiency of TM9SF1. The downregulated protein level of TM9SF1 enhance gastric cancer cell malignancy. And depletion of PCIF1 promotes the translation of its target mRNA TM9SF1. Ectopic TM9SF1 inhibits tumor growth and metastasis of gastric cancer cells. Data are shown as means ± SD. **P < 0.01, ***P < 0.001, Student’s t-test (c), Mann–Whitney test (e, f).