Correction: Colonization by Porphyromonas gingivalis in cervical squamous cell carcinomas promotes metastasis through FimA/CD151/ITGB1 signaling (Journal of Translational Medicine, (2025), 23, 1, (1166), 10.1186/s12967-025-06928-y)

Following publication of the original article [1], the authors reported an error in the Figures and Supplementary Material of the article. The Figures 1, 5 and 8 as well Supplementary Figures S2 and S3 included in Supplementary Material 3 were inadvertently not updated. All original raw data generated in this study have been deposited in the Research Data Deposit (RDD) platform of Sun Yat-sen University (http://www.researchdata.org.cn) under the registration ID RDDYJ745390. The incorrect version of Fig. 1 was: Porphyromonas gingivalis preferentially colonizes the tumor tissues of CSCC patients. A Representative images of immunohistochemical (IHC) staining of human CSCC tissues and the corresponding adjacent non-tumor tissues using an anti-P. gingivalis gingipain antibody. In the top row, the red dashed line indicates the tumor core region. The bottom row illustrates the spatial distribution of P. gingivalis in immune cell-enriched tumor tissues, showing that P. gingivalis predominantly localizes to the tumor core, with minimal colonization observed in the stromal areas and regions densely infiltrated by immune cells. Red arrows indicate immune cell-enriched regions. B Representative immunofluorescence images of P. gingivalis (green) in tumor tissues and adjacent non-tumor tissues of CSCC. DAPI (blue), cell nuclei. C Representative 16 S rRNA FISH images in tumor tissues and adjacent non-tumor tissues of CSCC. Porphyromonas gingivalis probe (green) is an FITC-conjugated oligonucleotide probe for P. gingivalis16S rRNA. EUB338 probe (red) is a Cy3-conjugated oligonucleotide probe for universal bacterial 16 S rRNA. DAPI (blue), cell nuclei. The white arrows indicate positive signals from P. gingivalis. D Quantitative analysis of FISH fluorescence intensity of the P. gingivalis probe in CSCC tissues and adjacent non-tumor tissues. E Overall survival was compared between P. gingivalis-negative and P. gingivalis-positive patients via the Kaplan–Meier method and log-rank test, *P < 0.05. The mean ± SEM is shown, **P < 0.01, *** P<0.001, **** P < 0.0001, two-tailed unpaired t-test The correct Fig. 1 is: Porphyromonas gingivalis preferentially colonizes the tumor tissues of CSCC patients. A Representative images of immunohistochemical (IHC) staining of human CSCC tissues and the corresponding adjacent non-tumor tissues using an anti-P. gingivalis gingipain antibody. In the top row, the red dashed line indicates the tumor core region. The bottom row illustrates the spatial distribution of P. gingivalis in immune cell-enriched tumor tissues, showing that P. gingivalis predominantly localizes to the tumor core, with minimal colonization observed in the stromal areas and regions densely infiltrated by immune cells. Red arrows indicate immune cell-enriched regions. B Representative immunofluorescence images of P. gingivalis (green) in tumor tissues and adjacent non-tumor tissues of CSCC. DAPI (blue), cell nuclei. C Representative 16 S rRNA FISH images in tumor tissues and adjacent non-tumor tissues of CSCC. Porphyromonas gingivalis probe (green) is an FITC-conjugated oligonucleotide probe for P. gingivalis16S rRNA. EUB338 probe (red) is a Cy3-conjugated oligonucleotide probe for universal bacterial 16 S rRNA. DAPI (blue), cell nuclei. The white arrows indicate positive signals from P. gingivalis. D Quantitative analysis of FISH fluorescence intensity of the P. gingivalis probe in CSCC tissues and adjacent non-tumor tissues. E Overall survival was compared between P. gingivalis-negative and P. gingivalis-positive patients via the Kaplan–Meier method and log-rank test, *P < 0.05. The mean ± SEM is shown, **P < 0.01, *** P<0.001, **** P < 0.0001, two-tailed unpaired t-test The incorrect version of Fig. 5 was: Porphyromonas gingivalis FimA selectively interacts with CD151/ITGB1 in CSCC cells. A Schematic diagram of the His pull-down assay. FimA, a major subunit of fimbriae of P. gingivalis, was overexpressed with a 6×His tag to pull down its corresponding receptors in SiHa cells. B SDS-PAGE and Western blot assays showing the recombinant His-FimA protein in E. coli. C Silver staining showing the candidate proteins that interact with His-FimA. D Mass spectrometry identification of potential protein interacting with FimA, and western blot analysis for the binding of FimA, ITGB1 and CD151 in His pull-down assay. E Expanded His pull-down assays to additional members of the tetraspanin and integrin families. F Validation of the interaction between FimA and CD151/ITGB1 by co-immunoprecipitation using anti-CD151 and anti-ITGB1 antibodies. G FimA was pulled down by the biotin-pull down assay of SiHa cell membrane proteins. H The basic protein levels of CD151 and ITGB1 in CSCC lines and HCECs were detected by Western blot assay. Compared with those in other CSCC lines and HCECs, CD151 and ITGB1 were overexpressed in SiHa cells. I, J STORM images showing that P. gingivalis (green) directly binds to CD151 (red) or ITGB1 (red) during adhesion to SiHa cells The correct Fig. 5 is: Porphyromonas gingivalis FimA selectively interacts with CD151/ITGB1 in CSCC cells. A Schematic diagram of the His pull-down assay. FimA, a major subunit of fimbriae of P. gingivalis, was overexpressed with a 6×His tag to pull down its corresponding receptors in SiHa cells. B SDS-PAGE and Western blot assays showing the recombinant His-FimA protein in E. coli. C Silver staining showing the candidate proteins that interact with His-FimA. D Mass spectrometry identification of potential protein interacting with FimA, and western blot analysis for the binding of FimA, ITGB1 and CD151 in His pull-down assay. E Expanded His pull-down assays to additional members of the tetraspanin and integrin families. F Validation of the interaction between FimA and CD151/ITGB1 by co-immunoprecipitation using anti-CD151 and anti-ITGB1 antibodies. G FimA was pulled down by the biotin-pull down assay of SiHa cell membrane proteins. H The basic protein levels of CD151 and ITGB1 in CSCC lines and HCECs were detected by Western blot assay. Compared with those in other CSCC lines and HCECs, CD151 and ITGB1 were overexpressed in SiHa cells. I, J STORM images showing that P. gingivalis (green) directly binds to CD151 (red) or ITGB1 (red) during adhesion to SiHa cells The incorrect version of Fig. 8 was: Porphyromonas gingivalis activates the JNK/Paxillin signaling pathway and regulates F-actin organization. A Volcano plot of the RNA sequencing dataset showing differentially expressed genes (DEGs) in SiHa cells treated with P. gingivalis (n=3) for 12 h (p < 0.05, fold change [FC]≥1.5). B KEGG pathway enrichment analysis of DEGs from the SiHa cell RNA sequencing dataset. C Porphyromonas gingivalis upregulated CD151 expression and activated JNK signalling in SiHa cells after 2 h and 4 h of coculture. Western blot analysis of JNK, p-JNK, Paxillin, p- Paxillin, CD151, and GAPDH expression. Band intensities were quantified and normalized to GAPDH; normalized relative expression levels (Target/GAPDH) are indicated below respective bands. D Representative SIM images of F-actin remodelling in SiHa cells induced by P. gingivalis. E Quantification of the maximum cell diameter. F Quantification of F-actin fluorescence intensity. SiHa cell was cocultured with CFSE-labelled bacteria (green; MOI=50) for 2, 4, and 6 h. F-actin: TRITC-phalloidin (red); Nuclei: DAPI (blue). G, HPorphyromonas gingivalis adhesion to SiHa cells depended on F-actin formation. I–K Migration and invasion mediated by P. gingivalis were abolished by depolymerization of F-actin in SiHa cells. Transwell assays were performed after 24 h The correct Fig. 8 is: Porphyromonas gingivalis activates the JNK/Paxillin signaling pathway and regulates F-actin organization. A Volcano plot of the RNA sequencing dataset showing differentially expressed genes (DEGs) in SiHa cells treated with P. gingivalis (n=3) for 12 h (p < 0.05, fold change [FC]≥1.5). B KEGG pathway enrichment analysis of DEGs from the SiHa cell RNA sequencing dataset. C Porphyromonas gingivalis upregulated CD151 expression and activated JNK signalling in SiHa cells after 2 h and 4 h of coculture. Western blot analysis of JNK, p-JNK, Paxillin, p- Paxillin, CD151, and GAPDH expression. Band intensities were quantified and normalized to GAPDH; normalized relative expression levels (Target/GAPDH) are indicated below respective bands. D Representative SIM images of F-actin remodelling in SiHa cells induced by P. gingivalis. E Quantification of the maximum cell diameter. F Quantification of F-actin fluorescence intensity. SiHa cell was cocultured with CFSE-labelled bacteria (green; MOI=50) for 2, 4, and 6 h. F-actin: TRITC-phalloidin (red); Nuclei: DAPI (blue). G, HPorphyromonas gingivalis adhesion to SiHa cells depended on F-actin formation. I–K Migration and invasion mediated by P. gingivalis were abolished by depolymerization of F-actin in SiHa cells. Transwell assays were performed after 24 h The Supplementary Material 3 has also been corrected in the original article. The original article [1] has been updated.