Cancer Research and Treatment

Erratum

ERRATUM: Caveolin-1 Modulates Docetaxel-Induced Cell Death in Breast Cancer Cell Subtypes through Different Mechanisms: Jinho Kang, Joo Hee Park, Hye Jin Lee, Ukhyun Jo, Jong Kuk Park, Jae Hong Seo, Yeul Hong Kim, Insun Kim, Kyong Hwa Park; Cancer Res Treat. 2019;51(3):1257-1257. Published online June 5, 2019; DOI: https://doi.org/10.4143/crt.2015.227.2; Corrects: Cancer Res Treat 2016;48(2):715

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Caveolin-1 Modulates Docetaxel-Induced Cell Death in Breast Cancer Cell Subtypes through Different Mechanisms: Jinho Kang, Joo Hee Park, Hye Jin Lee, Ukhyun Jo, Jong Kuk Park, Jae Hong Seo, Yeul Hong Kim, Insun Kim, Kyong Hwa Park; Cancer Res Treat. 2016;48(2):715-726. Published online September 21, 2015; DOI: https://doi.org/10.4143/crt.2015.227; Correction in: Cancer Res Treat 2019;51(3):1257

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Purpose
Caveolin-1 (CAV-1) expression is more associated with basal-like cancers than estrogen receptor- or ErbB-2–expressing breast cancers. However, the biological relevance of different levels of CAV-1 expression according to subtype in the epithelial compartment of breast cancer remains unclear.
Materials and Methods
We investigated whether CAV-1 functions as a tumor suppressor and/or modulator of the cytotoxic activity of docetaxel (DTX) in subtypes of breast cancer using in vitro and xenograft models.
Results
The levels of CAV-1 expression were closely associated with DTX sensitivity in triple-negative breast cancer cells. In addition, CAV-1 significantly inhibited cell proliferation and modulated DTX-induced apoptosis through cell cycle arrest in the G2/M phase. The mechanisms underlying DTX-induced apoptosis differed in breast cancers according to the levels of CAV- 1 expression. DTX robustly enhanced Bcl-2 inactivation by CAV-1 in MDA-MB-231 cells, while p53-mediated cell cycle arrest by DTX was more pronounced in CAV-1–low but p53-functional MCF-7 cells. In parallel with the data from breast cancer cell lines, CAV-1–transfected MCF-7 cells showed higher efficacy of DTX treatment in a xenograft model.
Conclusion
We clearly demonstrated cooperative effects between CAV-1 and DTX in mediating apoptosis, suggesting that the levels of CAV-1 expression might be an important indicator for DTX use in breast cancer.

Citations

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The Blocking of c-Met Signaling Induces Apoptosis through the Increase of p53 Protein in Lung Cancer: Hae-Yun Jung, Hyun-Jung Joo, Jong Kuk Park, Yeul Hong Kim; Cancer Res Treat. 2012;44(4):251-261. Published online December 31, 2012; DOI: https://doi.org/10.4143/crt.2012.44.4.251

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PURPOSE
c-Met is an attractive potential target for novel therapeutic inhibition of human cancer, and c-Met tyrosine kinase inhibitors (TKIs) are effective growth inhibitors of various malignancies. However, their mechanisms in anticancer effects are not clear. In the present study, we investigated the possibility that blocking c-Met signaling induces p53-mediated growth inhibition in lung cancer.
MATERIALS AND METHODS
The growth inhibitory effects of c-Met TKI (SU11274) on lung cancer cells and a xenograft model were assessed using the MTT assay, flow cytometry, and terminal deoxyribonucleotide transferase-mediated nick-end labeling staining. The role of p53 protein in the sensitivity of c-Met TKI (SU11274) was examined by Western blot analysis and immunohistochemistry.
RESULTS
SU11274 significantly induced apoptosis in A549 cells with wild-type p53, compared with that in Calu-1 cells with null-type p53. SU11274 increased p53 protein by enhancing the stability of p53 protein. Increased p53 protein by SU11274 induced up-regulation of Bax and PUMA expression and down-regulation of Bcl-2 expression, subsequently activating caspase 3. In p53 knock-out and knock-in systems, we confirmed that SU11274 caused apoptosis through the p53-mediated apoptotic pathway. Likewise, in the A549 xenograft model, SU11274 effectively shrank tumor volume and induced apoptosis via increased p53 protein expression. Blocking c-Met signaling increased the level of p53 protein.
CONCLUSION
Our finding suggested that p53 plays an important role in SU11274-induced apoptosis, and p53 status seems to be related to the sensitivity to SU11274 in lung cancer.

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