scholarly journals BMP4 Induces M2 Macrophage Polarization and Favors Tumor Progression in Bladder Cancer

2017 ◽  
Vol 23 (23) ◽  
pp. 7388-7399 ◽  
Author(s):  
Víctor G. Martínez ◽  
Carolina Rubio ◽  
Mónica Martínez-Fernández ◽  
Cristina Segovia ◽  
Fernando López-Calderón ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Tumor Progression ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization

Down-regulated paxillin suppresses cell proliferation and invasion by inhibiting M2 macrophage polarization in colon cancer

2018 ◽  
Vol 399 (11) ◽  
pp. 1285-1295 ◽  
Author(s):  
Ling-li Zhang ◽  
Lian-feng Zhang ◽  
Yun-bo Shi
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Tumor Progression ◽  
Macrophage Polarization ◽  
Enzyme Linked Immunosorbent Assay ◽  
M2 Macrophage ◽  
Akt Inhibitor ◽  
Endogenous Expression ◽  
M2 Macrophage Polarization ◽  
Proliferation And Invasion

Abstract The paxillin and M2 macrophage are all involved in cell proliferation and tumor progression, and this study aims to explore the interaction between them in colon cancer and the role of paxillin in cancer progression. Expression of mRNAs and proteins was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot, separately. Endogenous expression of genes was modulated by recombinant plasmids and cell transfection. The levels of cytokines were determined by enzyme-linked immunosorbent assay (ELISA). The cell viability, invasion and migration were detected using the MTT assay, the transwell assay and the wound-healing cell migration assay, respectively. A nude mouse model for human colon cancer was constructed for tumor orthotopic expression. Paxillin was up-regulated in tumor-associated macrophages (TAMs). Paxillin was up-regulated in process of M2 macrophage polarization. M2 macrophage polarization was inhibited with paxillin suppressed. Down-regulated paxillin inhibited cell proliferation and invasion in colon cancer through suppressing M2 macrophage polarization. PI3k/Akt inhibitor repressed M2 macrophage polarization through down-regulating paxillin. PI3k/Akt inhibitor inhibited the function of the macrophage in promoting cell proliferation and invasion of colon cancer through down-regulating paxillin. Down-regulated paxillin in macrophages inhibited tumor growth of colon cancer. With the PI3K/AKT pathway inhibited, down-regulated paxillin suppressed colon cancer cell proliferation and invasion by inhibiting the M2 macrophage polarization, thereby restraining the tumor progression.

scholarly journals MK2 contributes to tumor progression by promoting M2 macrophage polarization and tumor angiogenesis

2018 ◽  
Vol 115 (18) ◽  
pp. E4236-E4244 ◽  
Author(s):  
Lucia Suarez-Lopez ◽  
Ganapathy Sriram ◽  
Yi Wen Kong ◽  
Sandra Morandell ◽  
Karl A. Merrick ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Progression ◽  
Chronic Inflammation ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Colorectal Tumorigenesis ◽  
Tumor Neoangiogenesis ◽  
M2 Macrophage Polarization ◽  
Chemical Inhibition

Chronic inflammation is a major risk factor for colorectal cancer. The p38/MAPKAP Kinase 2 (MK2) kinase axis controls the synthesis of proinflammatory cytokines that mediate both chronic inflammation and tumor progression. Blockade of this pathway has been previously reported to suppress inflammation and to prevent colorectal tumorigenesis in a mouse model of inflammation-driven colorectal cancer, by mechanisms that are still unclear. Here, using whole-animal and tissue-specific MK2 KO mice, we show that MK2 activity in the myeloid compartment promotes tumor progression by supporting tumor neoangiogenesis in vivo. Mechanistically, we demonstrate that MK2 promotes polarization of tumor-associated macrophages into protumorigenic, proangiogenic M2-like macrophages. We further confirmed our results in human cell lines, where MK2 chemical inhibition in macrophages impairs M2 polarization and M2 macrophage-induced angiogenesis. Together, this study provides a molecular and cellular mechanism for the protumorigenic function of MK2.

scholarly journals Kdm6a Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with p53 Dysfunction

2020 ◽  
Vol 26 (8) ◽  
pp. 2065-2079 ◽  
Author(s):  
Kohei Kobatake ◽  
Ken-ichiro Ikeda ◽  
Yuichiro Nakata ◽  
Norimasa Yamasaki ◽  
Takeshi Ueda ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Inflammatory Pathways ◽  
M2 Macrophage Polarization

scholarly journals M2 macrophage polarization in chronic spontaneous urticaria refractory to antihistamine treatment

2021 ◽  
Author(s):  
Roberta F.J. Criado ◽  
Paulo Ricardo Criado ◽  
Carla Pagliari ◽  
Mirian N. Sotto ◽  
Carlos D'Apparecida Machado Filho ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Chronic Spontaneous Urticaria ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization

Nucleolin Improves Heart Function During Recovery From Myocardial Infarction by Modulating Macrophage Polarization

2021 ◽  
pp. 107424842198957
Author(s):  
Yuting Tang ◽  
Xiaofang Lin ◽  
Cheng Chen ◽  
Zhongyi Tong ◽  
Hui Sun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Early Phase ◽  
Heart Function ◽  
Macrophage Polarization ◽  
Late Phase ◽  
Macrophage Infiltration ◽  
Enzyme Linked Immunosorbent Assay ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization ◽  
Nucleolin Expression

Background: Nucleolin has multiple functions within cell survival and proliferation pathways. Our previous studies have revealed that nucleolin can significantly reduce myocardial ischemia-reperfusion injury by promoting myocardial angiogenesis and reducing myocardial apoptosis. In this study, we attempted to determine the role of nucleolin in myocardial infarction (MI) injury recovery and the underlying mechanism. Methods: Male BALB/c mice aged 6–8 weeks were used to set up MI models by ligating the left anterior descending coronary artery. Nucleolin expression in the heart was downregulated by intramyocardial injection of a lentiviral vector expressing nucleolin-specific small interfering RNA. Macrophage infiltration and polarization were measured by real-time polymerase chain reaction, flow cytometry, and immunofluorescence. Cytokines were detected by enzyme-linked immunosorbent assay. Results: Nucleolin expression in myocardium after MI induction decreased a lot at early phase and elevated at late phase. Nucleolin knockdown impaired heart systolic and diastolic functions and decreased the survival rate after MI. Macrophage infiltration increased in the myocardium after MI. Most macrophages belonged to the M1 phenotype at early phase (2 days) and the M2 phenotype increased greatly at late phase after MI. Nucleolin knockdown in the myocardium led to a decrease in M2 macrophage polarization with no effect on macrophage infiltration after MI. Furthermore, Notch3 and STAT6, key regulators of M2 macrophage polarization, were upregulated by nucleolin in RAW 264.7 macrophages. Conclusions: Lack of nucleolin impaired heart function during recovery after MI by reducing M2 macrophage polarization. This finding probably points to a new therapeutic option for ischemic heart disease.

Sign in / Sign up

Export Citation Format

Share Document