In this article, we found that there are some errors in Figures 1, 4 and 5. Therefore, we provide the correct version to replace the wrong figures and reflect changes. We sincerely apologize for this oversight and any confusion that may have caused. The corrected Figures 1, 4 and 5 are shown below.
Figure 1.
Downregulation of HSP105 expression in cSCC cells. (A) Real-time PCR and (B) Western blot analysis of HSP105 expression in HaCaT human keratinocytes and two cSCC cell lines (A431 and SCL-1). GAPDH was used as a loading control. (C) HSP105 overexpression and knockdown vectors and their negative controls were transfected with lentiviral efficiency up to 90%. HSP105 was stably overexpressed in LV-HSP105 cells compared to untreated and LV-con cells by (D) real-time PCR and (E) Western blot analysis. Stable knockdown of HSP105 expression in sh-HSP105 cells compared to untreated and sh-con cells by (F) real-time PCR and (G) Western blotting analysis. All results are presented as the mean ± SEM using one-way ANOVA in at least three independent experiments. **P < 0.01, ***P < 0.001, ****P < 0.0001, compared to the untreated group.
Figure 4.
HSP105 suppresses cSCC cell migration and invasion. (A) LV-HSP105 transfection resulted in a smaller migration area in A431 and SCL-1 cells. (B) Transwell assays showed that cell invasion was reduced after HSP105 overexpression. The results of (C) real-time PCR and (D) Western blot analysis showed reduced expression levels of MMP-2 and MMP-9 in the HSP105-overexpressing A431 and SCL-1 cells. (E) sh-HSP105 transfection resulted in a larger migration area in A431 and SCL-1 cells. (F) Enhanced cell invasion after HSP105 silencing. (G) Real-time PCR and (H) Western blot analysis showed elevated expression levels of MMP-2 and MMP-9 in A431 and SCL-1 cells with HSP105 knockdown. All results are presented as the mean ± SEM using one-way ANOVA in at least three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, compared to the untreated group.
Figure 5.
HSP105 suppresses cSCC cell growth by activating the MDM2/P53 signaling pathway. (A) Real-time PCR and (B) Western blot analysis showed that MDM2 protein levels were decreased and P53 protein levels were increased in A431 and SCL-1 cells after HSP105 overexpression. Moreover, CDK4 was downregulated, while the apoptosis-related protein Bax was upregulated and Bcl2 was downregulated. (C) Real-time PCR and (D) Western blot analysis showed the opposite results when HSP105 was knocked down. Co-IP (E) results show that there is an interaction between HSP105 and P53. The expression of HSP90 and HSP70 did not change in response to the elevation or knockdown (F) of HSP105.