Fig 2: SHB prescription effected proliferation and apoptosis of thyroid cells through regulated miR-511-3p/PTEN/PI3K/Akt pathway. (a) Protein expression of PTEN measured by western blotting. (b) Cell cycle distribution of FRTL-5 and Htori-3 measured by flow cytometry. (c) Cell viability rate of FRTL-5 and Htori-3 measured by CCK-8. (d) Cell apoptosis rate of FRTL-5 and Htori-3 measured by flow cytometry. (e) Expression of apoptosis-related proteins Bcl-2, Bax, and caspase-3 measured by western blotting. *P < 0.05 vs. normal group; **P < 0.01 vs. normal group; ***P < 0.001 vs. normal group; #P < 0.05 vs. blank group; ##P < 0.01 vs. blank group; ###P < 0.001 vs. blank group; ?P < 0.05 vs. 740 Y–P group; ??P < 0.01 vs. 740 Y–P group; ???P < 0.001 vs. 740 Y–P group.

Fig 3: TRIM55 overexpression suppresses cyclin D1 and c‐Myc. (A) Gene Ontology (GO) enrichment analysis of the top 800 genes with TRIM55‐activated or TRIM55‐Suppressed correlation coefficient. (B,C) Gene set enrichment analysis (GSEA) of the enriched signaling pathways with TRIM55‐High or TRIM‐55‐low expression using Hallmark signaling dataset. (D) SW620 and SW480 cells were transfected with empty vector or TRIM55‐OE. The protein expression levels of TRIM55, survivin, P27, p21/Cip1, Cyclin D1, c‐Myc, cleaved‐caspase 3, Bcl2, BAX, BAK, and GAPDH were examined by western blot. (E) IHC staining of c‐Myc and cyclin D1 was performed using SW620 xenograft tumor tissues. *p < 0.05, **p < 0.01, ***p < 0.001.

Fig 4: Identification and molecular docking verification of PBP anti-lung cancer core targets. (a) PPI network diagram obtained by STRING database analysis (interaction score > 0.9); (b) Visualizing the PPI network was completed using Cytoscape 3.9.1; (c) The docking mode of CASP3- osmundacetone, PARP-osmundacetone, TP53-osmundacetone, CASP3-hispidin, PARP-hispidin and TP53-hispidin.

Fig 5: Molecular mechanisms for overexpression of SELENBP1 inhibiting the malignant progression and inducing the apoptosis in NSCLC cells. Overexpression of SELENBP1 decreased the expression of PI3K, p‐PI3K, AKT, p‐AKT, mTOR, p‐mTOR, and Bcl‐2, whereas increased the expression of Bax and caspase‐3. Overexpression of SELENBP1 suppressed the malignant progression of NSCLC cells by inhibiting the PI3K/AKT/mTOR signaling. Moreover, overexpression of SELENBP1 inducing the apoptosis of NSCLC cells was associated with the activation of caspase‐3‐dependent axis under nonhigh level of oxidative stress. Furthermore, overexpression of SELENBP1 facilitating the cell apoptosis under high level of oxidative stress was related to its combining with GPX1 and colocalizing in nucleus (ROS, reactive oxygen species).