Yu, A. Y.H.A. Y.H.YuFu, R. H.R. H.FuSHAN-HUI HSUChiu, C. F.C. F.ChiuFang, W. H.W. H.FangYeh, C. A.C. A.YehTang, C. M.C. M.TangHsieh, H. H.H. H.HsiehHung, H. S.H. S.Hung2023-06-092023-06-092022-08-0125900498https://scholars.lib.ntu.edu.tw/handle/123456789/632009The authors regret for the wrong presentation of figures in Fig. 6B-c and Fig. S2A which may need to replace with the correct images. The authors would like to apologise for any inconvenience caused. 1. In Fig. 6.B, the BEAS-2B uptake images at 24 hr in subfigure (c) were misplaced. However, the semi-quantitative results from the images shown in subfigures (f) 24hr and (i) 24hr, are correct. Therefore, the authors have revised Fig. 6B-c to present the correct images below.2. In Fig. S2, the original images in subfigure (A) of BEAS-2B group were misplaced. The authors have provided the correct images for BEAS-2B group and presented the corrected Fig. S2A below.Fig. 6B. (continued).[Formula presented] Fig. 6. A. Assessment of endocytotic route for collagen gold on A549. Endocytosis acts an important role for cellular uptake, where F-actin plays a critical part. Several different types of endocytotic pathway have been proposed. The major involved mechanisms were caveolae, macropinocytosis, receptor-mediated endocytosis, and phagocytosis. Four kind of endocytotic inhibitors, CPZ, β-MCD, CCD, and Baf, were used to explore the entrance of the C–Au nanoparticles. The typical colocalization of C–Au with F-actin provides evidence for endocytotic entry process, which was substantially reduced after treating with endocytotic inhibitors from 30 min to 24 h (a–c), particularly for β-MCD and CPZ. The fluorescent intensity was measured by immunofluorescent method to quantify the inhibition effects (d–f). The amount, for β-MCD, decreased to 0.21-, 0.25-, 0.32-fold at 30 min, 2 h, and 24 h. Likewisely, for CPZ. For CCD and Baf, the inhibition amount was also decreased, respectively. The similar trend was observed by FACS determining (g–i). These findings indicate diversal route for endocytosis mediated C–Au entrance. Clathrin mediated and cholesterol dependent endocytosis may, however, play dominant role in terms of the particularly suppression effects. The potential route used by A549 for endocytosis and endosome-lysosomal transportation of the collagen gold nanoparticles (j). B. Assessment of endocytotic route for collagen gold on BEAS-2B. To explore what can it be different for cellular entry of nanoparticles between cancer and normal cells. We used endosomal inhibitors to treat BEAS-2B. In similar, the colocalization phenomenon of C–Au with F-actin can be observed from 30-min to 24-hr (a–c), and that can be also disturbed by endocytotic inhibitors, whereas Baf and CPZ posted stronger inhibition effects for BEAS-2B (a–c), different from β-MCD and CPZ for A549. The quantification using IF achieved 0.55-, 0.34-, and 0.30-fold for CPZ at 24 h (d–f), and that were 0.20-, 0.36-, and 0.29-fold by FACS (g–i). The inhibition trend remains consistent between IF and FACS. In terms of these findings, we sketched the potential uptake mechanisms of C–Au by BEAS-2B as shown in Fig. 6B–j. Fig. S2.[Formula presented][SDGs]SDG3corrigendum10.1016/j.mtadv.2022.1002752-s2.0-85135878593WOS:000862702000003https://api.elsevier.com/content/abstract/scopus_id/85135878593