Fig 1: miR-1307 inhibits autophagy and promotes the expression of oncogene dependent on the endoplasmic reticulum protein folding pathway(A) The total protein was extracted and analyzed by immunoprecipitation (IP). The samples were co-precipitated with anti-OSTC, and the precipitates were analyzed by western blotting with anti-ATG4. IgG immunoprecipitation was used as negative control.(B) The samples were co-precipitated with anti-CALR, and the precipitates were analyzed by western blotting with anti-ATG4.(C) The samples were co-immunoprecipitated with anti-ATG4, and the precipitates were analyzed by western blotting with anti-LC3.(D) The western blotting with anti-LC3. β-actin was used as the internal reference gene.(E) The samples were co-precipitated with anti-LC3, and the precipitates were analyzed by western blotting with anti-ATG3 and anti-ATG7.(F) The samples were co-immunoprecipitated with anti-ATG5, and the precipitates were analyzed by western blotting with anti-LC3, anti-ATG12, anti-ATG16l1, and anti-ATG9.(G) Western blotting with anti-beclin1. β-actin was used as the internal reference gene.(H) Autophagy LC3 HiBiT-reporter assay. The values of each group were expressed as mean ± SD (n = 3); ∗ ∗p < 0.01, ∗p < 0.05.(I) (a) Adenovirus Red-cherry-GFP-LC3 was infected, and autophagy was monitored. Autophagy was observed by fluorescence microscope (red marker cherry-LC3). (b) The incidence rate of autophagy was compared. Each experiment was repeated three times. The values of each group were expressed as mean ± SEM (n = 3); ∗ ∗p < 0.01, ∗p < 0.05.J&K. Western blotting analysis was performed using anti-PAK2, anti-PLK1, anti-PRKAR2A, anti-MYBL1, anti-Trim44, anti-Sash1, and anti-Smad5. β-actin was used as the internal reference gene.