Analysis of the relationship between resistin with prognosis, cell migration, and p38 and ERK1/2 activation in breast cancer

被引:0
|
作者
Cuachirria-Espinoza, Reyna L. [1 ]
Garcia-Miranda, Alin [1 ]
Hernandez-Barragan, Rafael [1 ]
Nava-Tapia, Dania A. [1 ]
Olea-Flores, Monserrat [1 ]
Navarro-Tito, Napoleon [1 ]
机构
[1] Univ Autonoma Guerrero, Fac Ciencias Quim Biol, Lab Biol Celular Canc, Ave Lazaro Cardenas S-N, Chilpancingo 39090, Gro, Mexico
关键词
Resistin; Prognosis; Cell migration; p38MAPK; ERK1/2; Breast cancer; EXPRESSION; SUBTYPES; TISSUE;
D O I
10.1016/j.biochi.2024.10.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Obesity increases the risk and mortality of breast cancer through dysregulated secretion of proinflammatory cytokines and tumor adipokines that induce an inflammatory breast microenvironment. Resistin is an adipokine secreted by adipocytes, immune cells, and predominantly macrophages, which contributes to cancer progression, but its molecular mechanism in cancer is not completely described. In this study, we analyzed the relationship of resistin on breast cancer prognosis and tumor progression and the effect in vitro of resistin on p38 and ERK1/2 activation in breast cancer cell lines. By bioinformatic analysis, we found that resistin is overexpressed in the basal subtype triple-negative breast cancer and is related to poor prognosis. In addition, we demonstrated a positive correlation between RETN and MAPK3 expression in basal triple-negative breast cancer. Importantly, we found amplifications of the RETN gene in at least 20 % of metastatic samples from patients with breast cancer. Most samples with RETN amplifications metastasized to bone and showed high expression of IL-8 (CXCL8) and IL-6 (IL6). Finally, resistin could be considered a prognostic marker for basal triple-negative breast cancer, and we also proposed the possibility that resistin-induced cell migration involves the activation of MAPK in breast cancer cells. (c) 2024 Elsevier B.V. and Soci & eacute;t & eacute; Fran & ccedil;aise de Biochimie et Biologie Mol & eacute;culaire (SFBBM). All rights are reserved, including those for text and data mining, AI training, and similar technologies.
引用
收藏
页码:19 / 29
页数:11
相关论文
共 50 条
  • [31] Involvement of ERK1/2 and p38 in Mg2+ accumulation in liver cells
    Lisa M. Torres
    Christie Cefaratti
    Beverly Perry
    Andrea Romani
    Molecular and Cellular Biochemistry, 2006, 288 : 191 - 199
  • [32] ERK1/2 and p38α/β Signaling in Tumor Cell Quiescence: Opportunities to Control Dormant Residual Disease
    Sosa, Maria Soledad
    Avivar-Valderas, Alvaro
    Bragado, Paloma
    Wen, Huei-Chi
    Aguirre-Ghiso, Julio A.
    CLINICAL CANCER RESEARCH, 2011, 17 (18) : 5850 - 5857
  • [33] Resistin promotes smooth muscle cell proliferation through activation of the ERK1/2 pathway
    Calabró, P
    Willerson, JT
    Yeh, ET
    EUROPEAN HEART JOURNAL, 2004, 25 : 126 - 127
  • [34] TGF-β1 modulates the homeostasis between MMPs and MMPs inhibitors through p38 MAPK and ERK1/2 in highly invasive human breast cancer cells
    Gomes, Luciana R.
    Terra, Leticia F.
    Wailemann, Rosangela A.
    Labriola, Leticia
    Sogayar, Mari C.
    CANCER RESEARCH, 2011, 71
  • [35] Amelogenin promotes odontoblast-like MDPC-23 cell differentiation via activation of ERK1/2 and p38 MAPK
    Yao, Naihui
    Li, Shiting
    Jiang, Yong
    Qiu, Songbo
    Tan, Yinghui
    MOLECULAR AND CELLULAR BIOCHEMISTRY, 2011, 355 (1-2) : 91 - 97
  • [36] Amelogenin promotes odontoblast-like MDPC-23 cell differentiation via activation of ERK1/2 and p38 MAPK
    Naihui Yao
    Shiting Li
    Yong Jiang
    Songbo Qiu
    Yinghui Tan
    Molecular and Cellular Biochemistry, 2011, 355 : 91 - 97
  • [37] HSP27 activates p38, ERK1, ERK2, but not JNK in human neutrophils
    Minielly, RC
    De, AK
    De, M
    Bankey, PE
    JOURNAL OF LEUKOCYTE BIOLOGY, 2004, : 30 - 30
  • [38] Effects of antiphospholipid antibodies on phosphorylation of p38 MAPK and ERK1/ERK2 in platelets.
    Vega-Ostertag, M
    Harris, EN
    Pierangeli, SS
    BLOOD, 2003, 102 (11) : 70B - 70B
  • [39] ERK1/2 and p38 pathways are required for P2Y receptor-mediated prostate cancer invasion
    Chen, L
    He, HY
    Li, HM
    Zheng, J
    Heng, WJ
    You, JF
    Fang, WG
    CANCER LETTERS, 2004, 215 (02) : 239 - 247
  • [40] Erk1/2 activation promotes compensated cardiac hypertrophy in transgenic mice while JNK1/2 or p38 activation promotes cardiomyopathy
    Bueno, OF
    De Windt, LJ
    Tymitz, KM
    Witt, SA
    Kimball, TR
    Klevitsky, R
    Hewett, TE
    Peng, CF
    Kitsis, RN
    Jones, SP
    Lefer, DJ
    Molkentin, JD
    CIRCULATION, 2000, 102 (18) : 288 - 288