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

Citations to this article as recorded by

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Docetaxel radiosensitizes castration-resistant prostate cancer by downregulating CAV-1
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International Journal of Radiation Biology.2024; 100(2): 256. CrossRef
Bio-Pathological Functions of Posttranslational Modifications of Histological Biomarkers in Breast Cancer
Anca-Narcisa Neagu, Claudiu-Laurentiu Josan, Taniya M. Jayaweera, Hailey Morrissiey, Kaya R. Johnson, Costel C. Darie
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Reports of Biochemistry and Molecular Biology.2023; 11(4): 532. CrossRef
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Nutrition and Cancer.2022; 74(1): 346. CrossRef
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AKAP12α is Associated with Promoter Methylation in Lung Cancer: Ukhyun Jo, Young Mi Whang, Han Kyeom Kim, Yeul Hong Kim; Cancer Res Treat. 2006;38(3):144-151. Published online June 30, 2006; DOI: https://doi.org/10.4143/crt.2006.38.3.144

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Purpose

Promoter methylation is an important mechanism for silencing tumor-suppressor genes in cancer and it is a promising tool for the development of molecular biomarkers. The purpose of the present study was to investigate whether inactivation of the A Kinase Anchoring Protein 12 (AKAP12) gene is assoCiated with promoter methylation in lung cancer.

Materials and Methods

The AKAP12 expression was examined by reverse transcription-polymerase chain reaction (RT-PCR) in ten lung cancer cell lines. The methylation status of the AKAP12α promoter was analyzed by performing bisulfite sequencing analysis in ten lung cancer cell lines, twenty four lung tissues and matched normal tissues.

Results

The AKAP12α expression was reduced in 6 of 10 (60%) lung cancer cell lines, whereas the AKAP12β expression was absent in 1 of 10 (10%) lung cancer cell lines. The AKAP12α expression was restored after treatment with the demethylating agent 5-aza-2'-deoxycytidine in three lung cancer cell lines. Methylation of CpG island 1 in the AKAP12α promoter was detected in 30% of the lung cancer cell lines, whereas methylation of CpG island 2 in the AKAP12α promoter was observed in the immortalized bronchial cell line and in all the lung cancer cell lines. In lung tumors, the CpG island 1 in the AKAP12α promoter was infrequently methylated. However, CpG island 2 in the AKAP12α promoter was highly methylated in lung tumors compared with the surrounding normal tissues, and this was statistically significant (p=0.0001).

Conclusion

Our results suggest that inactivation of the AKAP12α expression is assoCiated with DNA methylation of the promoter region in lung cancer, and that AKAP12α may play an important role in lung cancer carcinogenesis.

Citations

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