CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway
Although some breast cancer patients die due to tumor metastasis rather than from the primary tumor, the molecular mechanism of metastasis remains unclear. Therefore, it is necessary to inhibit breast cancer metastasis during cancer treatment. In this case, after designing and synthesizing CTI-2, we...
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| Format: | Article |
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MDPI AG
2021-11-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/22/12229 |
| _version_ | 1797509998732902400 |
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| author | Junfeng Ke Wenzhao Han Fanwei Meng Feng Guo Yuhong Wang Liping Wang |
| author_facet | Junfeng Ke Wenzhao Han Fanwei Meng Feng Guo Yuhong Wang Liping Wang |
| author_sort | Junfeng Ke |
| collection | DOAJ |
| description | Although some breast cancer patients die due to tumor metastasis rather than from the primary tumor, the molecular mechanism of metastasis remains unclear. Therefore, it is necessary to inhibit breast cancer metastasis during cancer treatment. In this case, after designing and synthesizing CTI-2, we found that CTI-2 treatment significantly reduced breast cancer cell metastasis in vivo and in vitro. Notably, with the treatment of CTI-2 in breast cancer cells, the expression level of E-cadherin increased, while the expression level of N-cadherin and vimentin decreased. In addition, after CTI-2 treatment, those outflow levels for p-ERK, p-p38, and p-JNK diminished, while no significant changes in the expression levels of ERK, JNK, or p38 were observed. Our conclusion suggested that CTI-2 inhibits the epithelial-mesenchymal transition (EMT) of breast carcinoma cells by inhibiting the activation of the mitogen-activated protein kinase (MAPK) signaling pathway, thereby inhibiting the metastasis of breast tumor cells. Therefore, we believe that CTI-2 is another candidate for breast tumor medication. |
| first_indexed | 2024-03-10T05:26:38Z |
| format | Article |
| id | doaj.art-76c7fe7952a64911a36554eb0253dfcd |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T05:26:38Z |
| publishDate | 2021-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-76c7fe7952a64911a36554eb0253dfcd2023-11-22T23:39:04ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-11-0122221222910.3390/ijms222212229CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling PathwayJunfeng Ke0Wenzhao Han1Fanwei Meng2Feng Guo3Yuhong Wang4Liping Wang5Key Laboratory for Molecular Enzymology and Engineering, Ministry of Education, Jilin University, Changchun 130012, ChinaKey Laboratory for Molecular Enzymology and Engineering, Ministry of Education, Jilin University, Changchun 130012, ChinaKey Laboratory for Molecular Enzymology and Engineering, Ministry of Education, Jilin University, Changchun 130012, ChinaKey Laboratory for Molecular Enzymology and Engineering, Ministry of Education, Jilin University, Changchun 130012, ChinaKey Laboratory for Molecular Enzymology and Engineering, Ministry of Education, Jilin University, Changchun 130012, ChinaKey Laboratory for Molecular Enzymology and Engineering, Ministry of Education, Jilin University, Changchun 130012, ChinaAlthough some breast cancer patients die due to tumor metastasis rather than from the primary tumor, the molecular mechanism of metastasis remains unclear. Therefore, it is necessary to inhibit breast cancer metastasis during cancer treatment. In this case, after designing and synthesizing CTI-2, we found that CTI-2 treatment significantly reduced breast cancer cell metastasis in vivo and in vitro. Notably, with the treatment of CTI-2 in breast cancer cells, the expression level of E-cadherin increased, while the expression level of N-cadherin and vimentin decreased. In addition, after CTI-2 treatment, those outflow levels for p-ERK, p-p38, and p-JNK diminished, while no significant changes in the expression levels of ERK, JNK, or p38 were observed. Our conclusion suggested that CTI-2 inhibits the epithelial-mesenchymal transition (EMT) of breast carcinoma cells by inhibiting the activation of the mitogen-activated protein kinase (MAPK) signaling pathway, thereby inhibiting the metastasis of breast tumor cells. Therefore, we believe that CTI-2 is another candidate for breast tumor medication.https://www.mdpi.com/1422-0067/22/22/12229breast cancermetastasisEMTMAPK |
| spellingShingle | Junfeng Ke Wenzhao Han Fanwei Meng Feng Guo Yuhong Wang Liping Wang CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway International Journal of Molecular Sciences breast cancer metastasis EMT MAPK |
| title | CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway |
| title_full | CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway |
| title_fullStr | CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway |
| title_full_unstemmed | CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway |
| title_short | CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway |
| title_sort | cti 2 inhibits metastasis and epithelial mesenchymal transition of breast cancer cells by modulating mapk signaling pathway |
| topic | breast cancer metastasis EMT MAPK |
| url | https://www.mdpi.com/1422-0067/22/22/12229 |
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