Key Takeaways & Executive Findings
- •• • Figure 2D (Transwell assay for MDA-MB-231 migration/invasion) was mislabeled; corrected panel now accurately reflects the original experimental results, ensuring that the reported CAV-1 deficiency effect on BCC invasion remains statistically supported at *P < 0.05, **P < 0.01, ***P < 0.001. • • Figure 4A (immunofluorescence for TGF-β1) contained a processing error; the corrected image confirms that CAV-1-deficient fibroblasts induce TGF-β1 secretion, a critical step in activating the TGF-β/Smad pathway, with significance thresholds of #P < 0.05, ##P < 0.01, ###P < 0.001. • • Figure 5A (scratch test for co-cultured BCCs) was mistakenly replaced; the corrected panel validates that SB431542 inhibits EMT and stemness in the CAV-1-deficient microenvironment, with statistical significance at ****P < 0.0001, reinforcing the therapeutic potential of TGF-β pathway inhibition. • • All corrections are strictly confined to figure presentation; the underlying data, statistical analyses (n = 3, mean ± SD), and main conclusions remain unaffected, preserving the study's clinical relevance for targeting CAV-1/TGF-β crosstalk in breast cancer.
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Abstract
This corrigendum addresses inaccuracies in three figure panels from the original article (Acta Biochim Biophys Sin 54: 1587–1598, doi: 10.3724/abbs.2022150). The authors identified that Figure 2D was mislabeled during preparation, Figure 4A contained an incorrect image due to a processing error, and Figure 5A was mistakenly replaced during final compilation. Corrected versions of these panels are provided. The authors confirm that these errors are confined to figure presentation and do not affect the underlying data, statistical analyses, or the main conclusions of the study. The original research demonstrated that caveolin-1 (CAV-1)-deficient fibroblasts promote migration, invasion, and stemness in breast cancer cells (BCCs) via activation of the TGF-β/Smad signaling pathway. Key experimental methods included Western blot for CAV-1 expression, scratch wound healing assays for migration, Transwell assays for migration and invasion, immunofluorescence and ELISA for TGF-β1 detection, and Western blot for EMT/stemness markers. Statistical significance was set at P < 0.05. This corrigendum ensures the accuracy of the scientific record and maintains the integrity of the reported findings.
1. Introduction
The original research identified a critical gap in understanding how the tumor microenvironment, specifically caveolin-1 (CAV-1)-deficient fibroblasts, drives breast cancer progression. Prior to this study, the mechanistic link between CAV-1 loss in stromal fibroblasts and enhanced migration, invasion, and stemness of breast cancer cells (BCCs) via TGF-β/Smad signaling was poorly defined. Existing commercial approaches targeting TGF-β signaling in breast cancer had shown limited efficacy due to off-target effects and incomplete pathway inhibition, necessitating a deeper investigation into the specific role of CAV-1 in fibroblast-mediated paracrine signaling.
This study employed a comprehensive experimental protocol including siRNA-mediated CAV-1 knockdown in fibroblasts, co-culture systems with MDA-MB-231 and MCF-7 BCCs, and functional assays (scratch, Transwell, immunofluorescence, ELISA, Western blot) to dissect the signaling cascade. The findings demonstrated that CAV-1 deficiency in fibroblasts induces TGF-β1 secretion, activating TGF-β/Smad signaling in BCCs and promoting malignant phenotypes. The corrigendum corrects figure presentation errors in Figures 2D, 4A, and 5A, ensuring the accuracy of the scientific record without altering the validated conclusions.
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Qingyun Huang, Longyuan Wu, Yi Wang, Xinyu Kong, Xinhua Xiao, Qiyuan Huang, Miao Li, Yujia Zhai, Fuxiu Shi, Ruichen Zhao, Junpei Zhong, Lixia Xiong (2025). Corrigendum to 'Caveolin-1-deficient fibroblasts promote migration, invasion, and stemness by activating the TGF-β/Smad signaling pathway in breast cancer cells'. Acta Biochimica et Biophysica Sinica. https://doi.org/10.3724/abbs.2025233
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Frequently Asked Questions
What specific errors were identified in the original figures, and how were they corrected?
Three errors were identified: Figure 2D was mislabeled during preparation, Figure 4A contained an incorrect image due to a processing error, and Figure 5A was mistakenly replaced during final compilation. Corrected versions of these panels are provided in the corrigendum. The authors verified that these errors were confined to figure presentation and did not affect the underlying data, statistical analysis (n = 3, mean ± SD, significance at P < 0.05), or main conclusions.
Do these corrections impact the statistical significance or conclusions of the original study?
No. The authors confirm that the errors are strictly confined to figure presentation. The underlying data, statistical analyses (including significance thresholds such as *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, #P < 0.05, ##P < 0.01, ###P < 0.001, +P < 0.05, ++P < 0.01, +++P < 0.001), and main conclusions remain unaffected. The corrected figures accurately represent the experimental results, ensuring the integrity of the reported findings.
What are the key experimental methods used in the original study to assess migration, invasion, and stemness?
The study employed cell scratch tests to measure migration of MDA-MB-231 and MCF-7 cells, Transwell assays to assess migration and invasion, immunofluorescence staining and ELISA to detect TGF-β1 expression and secretion, and Western blot to measure TGF-β1, TGF-βR2, p-Smad, Smad, and EMT/stemness-related proteins. All assays were performed with n = 3, and data are presented as mean ± SD with statistical significance set at P < 0.05.
How does the CAV-1-deficient fibroblast microenvironment promote breast cancer progression, and what is the role of SB431542?
CAV-1-deficient fibroblasts induce TGF-β1 secretion, which activates the TGF-β/Smad signaling pathway in breast cancer cells, promoting migration, invasion, and stemness. SB431542, a TGF-β receptor inhibitor, was shown to inhibit EMT and stemness in co-cultured BCCs within the CAV-1-deficient microenvironment by blocking this pathway. This was demonstrated through scratch tests, Transwell assays, and Western blot analysis of EMT/stemness markers and signaling proteins (Smad and p-Smad), with statistical significance at ****P < 0.0001.
What are the clinical implications of targeting the CAV-1/TGF-β axis in breast cancer?
The findings suggest that CAV-1 loss in stromal fibroblasts creates a pro-tumorigenic microenvironment via TGF-β1 secretion, which can be therapeutically targeted. Inhibiting TGF-β signaling with agents like SB431542 reduces EMT and stemness in breast cancer cells, offering a potential strategy to counteract CAV-1 deficiency-driven progression. However, further in vivo studies are needed to validate efficacy and safety, as the current data are based on in vitro co-culture models with n = 3 and statistical significance at P < 0.05.
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