Fibronectin expression is upregulated by PI-3K/Akt activation in tamoxifen-resistant breast cancer cells
Fibronectin (FN) plays important roles in the EMT in a variety of cancer cell types. However, the mechanism by which FN expression is regulated in tamoxifen-resistant (TamR) breast cancer cells has not yet been fully elucidated. Aberrant FN expression was associated with poor prognosis in patients w...
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Published in | BMB reports Vol. 50; no. 12; pp. 615 - 620 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
Korean Society for Biochemistry and Molecular Biology
01.12.2017
생화학분자생물학회 |
Subjects | |
Online Access | Get full text |
ISSN | 1976-6696 1976-670X |
DOI | 10.5483/bmbrep.2017.50.12.096 |
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Abstract | Fibronectin (FN) plays important roles in the EMT in a variety of cancer cell types. However, the mechanism by which FN expression is regulated in tamoxifen-resistant (TamR) breast cancer cells has not yet been fully elucidated. Aberrant FN expression was associated with poor prognosis in patients with luminal type A breast cancer. In addition, FN was upregulated in TamR cells. To investigate the mechanism by which FN expression is regulated, we assessed the levels of phosphorylated Akt, JNK, and STAT3 and found that they were all increased in TamR cells. Induction of FN expression was dampened by LY294002 or AKT IV in TamR cells. Furthermore, FN expression was increased by constitutively active (CA)-Akt overexpression in tamoxifen-sensitive MCF7 (TamS) cells and colony formation of TamR cells was blocked by AKT IV treatment. Taken together, these results demonstrate that FN expression is upregulated through the PI-3K/Akt pathway in tamoxifen-resistant breast cancer cells. [BMB Reports 2017; 50(12): 615-620]. |
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AbstractList | Fibronectin (FN) plays important roles in the EMT in a variety of cancer cell types. However, the mechanism by which FN expression is regulated in tamoxifen-resistant (TamR) breast cancer cells has not yet been fully elucidated. Aberrant FN expression was associated with poor prognosis in patients with luminal type A breast cancer. In addition, FN was upregulated in TamR cells. To investigate the mechanism by which FN expression is regulated, we assessed the levels of phosphorylated Akt, JNK, and STAT3 and found that they were all increased in TamR cells. Induction of FN expression was dampened by LY294002 or AKT IV in TamR cells. Furthermore, FN expression was increased by constitutively active (CA)-Akt overexpression in tamoxifen-sensitive MCF7 (TamS) cells and colony formation of TamR cells was blocked by AKT IV treatment. Taken together, these results demonstrate that FN expression is upregulated through the PI-3K/Akt pathway in tamoxifen-resistant breast cancer cells. [BMB Reports 2017; 50(12): 615-620]. Fibronectin (FN) plays important roles in the EMT in a variety of cancer cell types. However, the mechanism by which FN expression is regulated in tamoxifen-resistant (TamR) breast cancer cells has not yet been fully elucidated. Aberrant FN expression was associated with poor prognosis in patients with luminal type A breast cancer. In addition, FN was upregulated in TamR cells. To investigate the mechanism by which FN expression is regulated, we assessed the levels of phosphorylated Akt, JNK, and STAT3 and found that they were all increased in TamR cells. Induction of FN expression was dampened by LY294002 or AKT IV in TamR cells. Furthermore, FN expression was increased by constitutively active (CA)-Akt overexpression in tamoxifen-sensitive MCF7 (TamS) cells and colony formation of TamR cells was blocked by AKT IV treatment. Taken together, these results demonstrate that FN expression is upregulated through the PI-3K/Akt pathway in tamoxifen-resistant breast cancer cells. KCI Citation Count: 5 Fibronectin (FN) plays important roles in the EMT in a variety of cancer cell types. However, the mechanism by which FN expression is regulated in tamoxifen-resistant (TamR) breast cancer cells has not yet been fully elucidated. Aberrant FN expression was associated with poor prognosis in patients with luminal type A breast cancer. In addition, FN was upregulated in TamR cells. To investigate the mechanism by which FN expression is regulated, we assessed the levels of phosphorylated Akt, JNK, and STAT3 and found that they were all increased in TamR cells. Induction of FN expression was dampened by LY294002 or AKT IV in TamR cells. Furthermore, FN expression was increased by constitutively active (CA)-Akt overexpression in tamoxifen-sensitive MCF7 (TamS) cells and colony formation of TamR cells was blocked by AKT IV treatment. Taken together, these results demonstrate that FN expression is upregulated through the PI-3K/Akt pathway in tamoxifen-resistant breast cancer cells. |
Author | Kim, Sangmin You, Daeun Jeong, Yisun Jung, Seung Pil Bae, Soo Youn Lee, Jeong Eon |
AuthorAffiliation | 2 Departments of Surgery, Samsung Medical Center, Seoul 06351, Korea 1 Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea 3 Breast Cancer Center, Samsung Medical Center, Seoul 06351, Korea 4 Division of Breast and Endocrine Surgery, Department of Surgery, Korea University Hospital, Korea University College of Medicine, Seoul 02852, Korea |
AuthorAffiliation_xml | – name: 1 Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea – name: 3 Breast Cancer Center, Samsung Medical Center, Seoul 06351, Korea – name: 2 Departments of Surgery, Samsung Medical Center, Seoul 06351, Korea – name: 4 Division of Breast and Endocrine Surgery, Department of Surgery, Korea University Hospital, Korea University College of Medicine, Seoul 02852, Korea |
Author_xml | – sequence: 1 givenname: Daeun surname: You fullname: You, Daeun organization: Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea – sequence: 2 givenname: Seung Pil surname: Jung fullname: Jung, Seung Pil organization: Division of Breast and Endocrine Surgery, Department of Surgery, Korea University Hospital, Korea University College of Medicine, Seoul 02852, Korea – sequence: 3 givenname: Yisun surname: Jeong fullname: Jeong, Yisun organization: Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea – sequence: 4 givenname: Soo Youn surname: Bae fullname: Bae, Soo Youn organization: Division of Breast and Endocrine Surgery, Department of Surgery, Korea University Hospital, Korea University College of Medicine, Seoul 02852, Korea – sequence: 5 givenname: Jeong Eon surname: Lee fullname: Lee, Jeong Eon organization: Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea; Departments of Surgery, and Breast Cancer Center, Samsung Medical Center, Seoul 06351, Korea – sequence: 6 givenname: Sangmin surname: Kim fullname: Kim, Sangmin organization: Breast Cancer Center, Samsung Medical Center, Seoul 06351, Korea |
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CitedBy_id | crossref_primary_10_3390_cancers14010214 crossref_primary_10_1002_jcp_31048 crossref_primary_10_3390_cancers12102870 crossref_primary_10_3390_cancers15164145 crossref_primary_10_1186_s12935_021_02312_0 crossref_primary_10_3389_fonc_2022_1019025 crossref_primary_10_5483_BMBRep_2018_51_8_105 crossref_primary_10_1186_s12935_024_03541_9 crossref_primary_10_3390_cancers12051173 crossref_primary_10_1042_CS20220284 crossref_primary_10_3892_ijo_2019_4679 crossref_primary_10_1016_j_isci_2022_105501 crossref_primary_10_1186_s12964_020_00580_3 crossref_primary_10_1016_j_abb_2024_110173 crossref_primary_10_1038_s41419_025_07367_9 crossref_primary_10_1369_0022155420930112 |
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Copyright | Copyright © 2017 by the The Korean Society for Biochemistry and Molecular Biology 2017 |
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Snippet | Fibronectin (FN) plays important roles in the EMT in a variety of cancer cell types. However, the mechanism by which FN expression is regulated in... |
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SubjectTerms | Antineoplastic Agents, Hormonal - chemistry Antineoplastic Agents, Hormonal - pharmacology Breast Neoplasms - drug therapy Breast Neoplasms - metabolism Breast Neoplasms - pathology Drug Resistance, Neoplasm - drug effects Female Fibronectins - biosynthesis Fibronectins - genetics Fibronectins - metabolism Humans MCF-7 Cells Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Real-Time Polymerase Chain Reaction Tamoxifen - chemistry Tamoxifen - pharmacology Tumor Cells, Cultured Up-Regulation - drug effects 화학 |
Title | Fibronectin expression is upregulated by PI-3K/Akt activation in tamoxifen-resistant breast cancer cells |
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