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...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Junfeng Ke, Wenzhao Han, Fanwei Meng, Feng Guo, Yuhong Wang, Liping Wang
Formato: article
Lenguaje:EN
Publicado: MDPI AG 2021
Materias:
EMT
Acceso en línea:https://doaj.org/article/76c7fe7952a64911a36554eb0253dfcd
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:76c7fe7952a64911a36554eb0253dfcd
record_format dspace
spelling oai:doaj.org-article:76c7fe7952a64911a36554eb0253dfcd2021-11-25T17:54:32ZCTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway10.3390/ijms2222122291422-00671661-6596https://doaj.org/article/76c7fe7952a64911a36554eb0253dfcd2021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12229https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Although 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.Junfeng KeWenzhao HanFanwei MengFeng GuoYuhong WangLiping WangMDPI AGarticlebreast cancermetastasisEMTMAPKBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12229, p 12229 (2021)
institution DOAJ
collection DOAJ
language EN
topic breast cancer
metastasis
EMT
MAPK
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle breast cancer
metastasis
EMT
MAPK
Biology (General)
QH301-705.5
Chemistry
QD1-999
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
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.
format article
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
title 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_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_sort cti-2 inhibits metastasis and epithelial-mesenchymal transition of breast cancer cells by modulating mapk signaling pathway
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/76c7fe7952a64911a36554eb0253dfcd
work_keys_str_mv AT junfengke cti2inhibitsmetastasisandepithelialmesenchymaltransitionofbreastcancercellsbymodulatingmapksignalingpathway
AT wenzhaohan cti2inhibitsmetastasisandepithelialmesenchymaltransitionofbreastcancercellsbymodulatingmapksignalingpathway
AT fanweimeng cti2inhibitsmetastasisandepithelialmesenchymaltransitionofbreastcancercellsbymodulatingmapksignalingpathway
AT fengguo cti2inhibitsmetastasisandepithelialmesenchymaltransitionofbreastcancercellsbymodulatingmapksignalingpathway
AT yuhongwang cti2inhibitsmetastasisandepithelialmesenchymaltransitionofbreastcancercellsbymodulatingmapksignalingpathway
AT lipingwang cti2inhibitsmetastasisandepithelialmesenchymaltransitionofbreastcancercellsbymodulatingmapksignalingpathway
_version_ 1718411869719363584