C–C Chemokine Ligand 2 (CCL2) Recruits Macrophage-Membrane-Camouflaged Hollow Bismuth Selenide Nanoparticles To Facilitate Photothermal Sensitivity and Inhibit Lung Metastasis of Breast Cancer

2018 ◽  
Vol 10 (37) ◽  
pp. 31124-31135 ◽  
Author(s):  
Hongjuan Zhao ◽  
Li Li ◽  
Junli Zhang ◽  
Cuixia Zheng ◽  
Kaili Ding ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Lung Metastasis ◽  
Bismuth Selenide ◽  
Chemokine Ligand ◽  
Chemokine Ligand 2 ◽  
Macrophage Membrane

scholarly journals CCL2-induced chemokine cascade promotes breast cancer metastasis by enhancing retention of metastasis-associated macrophages

2015 ◽  
Vol 212 (7) ◽  
pp. 1043-1059 ◽  
Author(s):  
Takanori Kitamura ◽  
Bin-Zhi Qian ◽  
Daniel Soong ◽  
Luca Cassetta ◽  
Roy Noy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Lung Metastasis ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Inflammatory Monocytes ◽  
Chemokine Ligand ◽  
Cc Chemokine Ligand 2 ◽  
Chemokine Ligand 2

Pulmonary metastasis of breast cancer cells is promoted by a distinct population of macrophages, metastasis-associated macrophages (MAMs), which originate from inflammatory monocytes (IMs) recruited by the CC-chemokine ligand 2 (CCL2). We demonstrate here that, through activation of the CCL2 receptor CCR2, the recruited MAMs secrete another chemokine ligand CCL3. Genetic deletion of CCL3 or its receptor CCR1 in macrophages reduces the number of lung metastasis foci, as well as the number of MAMs accumulated in tumor-challenged lung in mice. Adoptive transfer of WT IMs increases the reduced number of lung metastasis foci in Ccl3 deficient mice. Mechanistically, Ccr1 deficiency prevents MAM retention in the lung by reducing MAM–cancer cell interactions. These findings collectively indicate that the CCL2-triggered chemokine cascade in macrophages promotes metastatic seeding of breast cancer cells thereby amplifying the pathology already extant in the system. These data suggest that inhibition of CCR1, the distal part of this signaling relay, may have a therapeutic impact in metastatic disease with lower toxicity than blocking upstream targets.

Tumor-targeted gene therapy with lipid nanoparticles inhibits tumor-associated adipocytes and remodels the immunosuppressive tumor microenvironment in triple-negative breast cancer

2021 ◽  
Vol 6 (4) ◽  
pp. 319-329
Author(s):  
Yun Liu ◽  
Karthik Tiruthani ◽  
Menglin Wang ◽  
Xuefei Zhou ◽  
Nasha Qiu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Microenvironment ◽  
Triple Negative ◽  
Lipid Nanoparticles ◽  
Cancer Model ◽  
Breast Cancer Model ◽  
Chemokine Ligand ◽  
Immunosuppressive Tumor Microenvironment ◽  
Targeted Gene Therapy ◽  
Chemokine Ligand 2

In breast cancer model, we identified C–C Motif Chemokine Ligand 2 (CCL2) as the key mediator which is secreted by tumor associated adipocytes, and developed targeted lipid-protamine-DNA (LPD) nanoparticles to locally “trap” CCL2 to ameliorate the immunosuppressive tumor microenvironment.

Liposomes Coated with Isolated Macrophage Membrane Can Target Lung Metastasis of Breast Cancer

ACS Nano ◽  
2016 ◽  
Vol 10 (8) ◽  
pp. 7738-7748 ◽  
Author(s):  
Haiqiang Cao ◽  
Zhaoling Dan ◽  
Xinyu He ◽  
Zhiwen Zhang ◽  
Haijun Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Lung Metastasis ◽  
Macrophage Membrane

CDK12 Promotes Breast Cancer Progression and Maintains Stemness by Activating c-myc/β -catenin Signaling

2020 ◽  
Vol 20 (2) ◽  
pp. 156-165 ◽  
Author(s):  
Fang Peng ◽  
Chuansheng Yang ◽  
Yanan Kong ◽  
Xiaojia Huang ◽  
Yanyu Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Lung Metastasis ◽  
Xenograft Model ◽  
Breast Cancer Cell Lines ◽  
Cell Renewal ◽  
Cancer Stemness ◽  
Mesenchymal Transition ◽  
Potential Biomarker

Background: CDK12 is a promising therapeutic target in breast cancer with an effective ability of maintaining cancer cell stemness. Objective: We aim to investigate the mechanism of CDK12 in maintaining breast cancer stemness. Methods: CDK12 expression level was accessed by using RT-qPCR and IHC. CDK12-altered breast cancer cell lines MDA-MB-231-shCDK12 and SkBr-3-CDK12 were then established. CCK8, colony formation assays, and xenograft model were used to value the effect of CDK12 on tumorigenicity. Transwell assay, mammosphere formation, FACS, and lung metastasis model in vivo were determined. Western blot further characterized the mechanism of CDK12 in breast cancer stemness through the c-myc/β-catenin pathway. Results: Our results showed a higher level of CDK12 exhibited in breast cancer samples. Tumor formation, cancer cell mobility, spheroid forming, and the epithelial-mesenchymal transition will be enhanced in the CDK12high group. In addition, CDK12 was associated with lung metastasis and maintained breast cancer cell stemness. CDK12high cancer cells presented higher tumorigenicity and a population of CD44+ subset compared with CDK12low cells. Our study demonstrated c-myc positively expressed with CDK12. The c-myc/β-catenin signaling was activated by CDK12, which is a potential mechanism to initiate breast cancer stem cell renewal and may serve as a potential biomarker of breast cancer prognosis. Conclusion: CDK12 overexpression promotes breast cancer tumorigenesis and maintains the stemness of breast cancer by activating c-myc/β-catenin signaling. Inhibiting CDK12 expression may become a potential therapy for breast cancer.

scholarly journals Entelon® (Vitis vinifera Seed Extract) Prevents Cancer Metastasis via the Downregulation of Interleukin-1 Alpha in Triple-Negative Breast Cancer Cells

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3644
Author(s):  
Daeun You ◽  
Yisun Jeong ◽  
Sun Young Yoon ◽  
Sung A Kim ◽  
Eunji Lo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Lung Metastasis ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Interleukin 1 ◽  
Metastatic Potential ◽  
Cancer Cell Proliferation ◽  
Dependent Pathway

Interleukin-1 (IL1) is a proinflammatory cytokine and promotes cancer cell proliferation and invasiveness in a diversity of cancers, such as breast and colon cancer. Here, we focused on the pharmacological effect of Entelon® (ETL) on the tumorigenesis of triple-negative breast cancer (TNBC) cells by IL1-alpha (IL1A). IL1A enhanced the cell growth and invasiveness of TNBC cells. We observed that abnormal IL1A induction is related with the poor prognosis of TNBC patients. IL1A also increased a variety of chemokines such as CCL2 and IL8. Interestingly, IL1A expression was reduced by the ETL treatment. Here, we found that ETL significantly decreased the MEK/ERK signaling pathway in TNBC cells. IL1A expression was reduced by UO126. Lastly, we studied the effect of ETL on the metastatic potential of TNBC cells. Our results showed that ETL significantly reduced the lung metastasis of TNBC cells. Our results showed that IL1A expression was regulated by the MEK/ERK- and PI3K/AKT-dependent pathway. Taken together, ETL inhibited the MEK/ERK and PI3K/AKT signaling pathway and suppressing the lung metastasis of TNBC cells through downregulation of IL1A. Therefore, we propose the possibility of ETL as an effective adjuvant for treating TNBC.

scholarly journals Macrophage Migration Inhibitory Factor Induces Macrophage Recruitment via CC Chemokine Ligand 2

2006 ◽  
Vol 177 (11) ◽  
pp. 8072-8079 ◽  
Author(s):  
Julia L. Gregory ◽  
Eric F. Morand ◽  
Sonja J. McKeown ◽  
Jennifer A. Ralph ◽  
Pamela Hall ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Cc Chemokine ◽  
Macrophage Recruitment ◽  
Chemokine Ligand ◽  
Cc Chemokine Ligand 2 ◽  
Chemokine Ligand 2
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