CC chemokine ligand 21 enhances the immunogenicity of the breast cancer cell line MCF-7 upon assistance of TLR2

Wu, Shao-Guo; Lu, Xinyu; Zhang, Z. L.; Lei, Ping; Hu, Ping; Wang, M.; Huang, Bo; Wei, Xing; Jiang, Xiaotao; Liu, H. J.; Zhu, Zhigang; Li, W. H.; Zhu, Huaqing; Fu, Ning; Shen, Guanxin

doi:10.1093/carcin/bgq265

Cited by 22 publications

(22 citation statements)

References 28 publications

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“…46 Indeed, a recent study showed that TLR2 activation promotes breast cancer cell invasiveness and adhesiveness. 52 Moreover, in a melanoma mouse model, TLR2 targeting attenuates pulmonary metastases of tumor, whereas combining an anti-TLR2 antibody and a cytotoxic agent, gemcitabine, provided a further improvement in the survival of tumor-bearing mice. 53 Remarkably, TLR2 stimulation has been shown to sense oxidation-associated molecular patterns, providing a key link connecting inflammation, oxidative stress and innate immunity.…”

Section: Methodsmentioning

confidence: 99%

TLR2 enhances ovarian cancer stem cell self-renewal and promotes tumor repair and recurrence

et al. 2013

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Primary ovarian cancer is responsive to treatment, but chemoresistant recurrent disease ensues in majority of patients. Recent compelling evidence demonstrates that a specific population of cancer cells, the cancer stem cells, initiates and sustains tumors. It is therefore possible that this cell population is also responsible for recurrence. We have shown previously that CD44+/MyD88+ epithelial ovarian cancer stem cells (CD44+/MyD88+ EOC stem cells) are responsible for tumor initiation. In this study, we demonstrate that this population drives tumor repair following surgery- and chemotherapy-induced tumor injury. Using in vivo and in vitro models, we also demonstrate that during the process of tumor repair, CD44+/MyD88+ EOC stem cells undergo self-renewal as evidenced by upregulation of stemness-associated genes. More importantly, we show that a pro-inflammatory microenvironment created by the TLR2-MyD88-NFκB pathway supports EOC stem cell-driven repair and self-renewal. Overall, our findings point to a specific cancer cell population, the CD44+/MyD88+ EOC stem cells and a specific pro-inflammatory pathway, the TLR2-MyD88-NFκB pathway, as two of the required players promoting tumor repair, which is associated with enhanced cancer stem cell load. Identification of these key players is the first step in elucidating the steps necessary to prevent recurrence in EOC patients.

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Section: Methodsmentioning

confidence: 99%

TLR2 enhances ovarian cancer stem cell self-renewal and promotes tumor repair and recurrence

et al. 2013

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“…This process is dependent on the receptor of these chemokines: CCR7 [ 2 , 190 ]. Therefore, the increased expression of these chemokines in a tumor has an anti-cancer effect via cytotoxic TIL [ 195 , 196 , 197 , 198 ].…”

Section: Ccr7 Ccl19 and Ccl21mentioning

confidence: 99%

CC Chemokines in a Tumor: A Review of Pro-Cancer and Anti-Cancer Properties of Receptors CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10 Ligands

Korbecki

Grochans

Gutowska

et al. 2020

IJMS

221

176

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CC chemokines (or β-chemokines) are 28 chemotactic cytokines with an N-terminal CC domain that play an important role in immune system cells, such as CD4+ and CD8+ lymphocytes, dendritic cells, eosinophils, macrophages, monocytes, and NK cells, as well in neoplasia. In this review, we discuss human CC motif chemokine ligands: CCL1, CCL3, CCL4, CCL5, CCL18, CCL19, CCL20, CCL21, CCL25, CCL27, and CCL28 (CC motif chemokine receptor CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10 ligands). We present their functioning in human physiology and in neoplasia, including their role in the proliferation, apoptosis resistance, drug resistance, migration, and invasion of cancer cells. We discuss the significance of chemokine receptors in organ-specific metastasis, as well as the influence of each chemokine on the recruitment of various cells to the tumor niche, such as cancer-associated fibroblasts (CAF), Kupffer cells, myeloid-derived suppressor cells (MDSC), osteoclasts, tumor-associated macrophages (TAM), tumor-infiltrating lymphocytes (TIL), and regulatory T cells (Treg). Finally, we show how the effect of the chemokines on vascular endothelial cells and lymphatic endothelial cells leads to angiogenesis and lymphangiogenesis.

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“…The interaction between CCR7 and CCL21 has been shown to improve the immunogenicity of CCR7-expressing breast cancer cells [85]. It also induces actin polymerization and pseudopodia formation, resulting in increased cell motility as illustrated in (Figure 1) [86].…”

Section: C-c Chemokine Receptor 7 (Ccr7) and Breast Cancermentioning

confidence: 99%

“…Indeed, in vivo CCR7 C-terminal partial truncation decreases the receptor internalization, while maintaining the chemotaxis ability to CCR7 ligands [135], and prevents lymphocyte adhesion and extravasation to the HEVs [136]. Additional studies reported that the intra-tumoral injection of recombinant CCL21 significantly delayed tumor progression and stimulated cytotoxic immune responses [85,137]. Moreover, in vitro experiments have demonstrated that blocking the CCR7 receptor decreases the incidence of metastasis [86,121].…”

Section: Therapy and Future Directionsmentioning

confidence: 99%

The Role of CCL21/CCR7 Chemokine Axis in Breast Cancer Progression

Rizeq

Malki

2020

Cancers

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Breast cancer is a leading cause of cancer-related deaths worldwide, predominantly caused by metastasis. It is generally accepted that the pattern of breast cancer metastasis is largely determined by the interaction between the chemokine receptors on cancer cells and the chemokines expressed at the sites of metastatic disease. Chemokine receptors belong to the G-protein-coupled receptors (GPCRs) family that appear to be implicated in inflammatory diseases, tumor growth and metastasis. One of its members, C-C Chemokine receptor 7 (CCR7), binds chemokines CCL19 and CCL21, which are important for tissue homeostasis, immune surveillance and tumorigenesis. These receptors have been shown to induce the pathobiology of breast cancer due to their ability to induce cellular proliferation and migration upon the binding of the cognate chemokine receptors. The underlying signaling pathways and exact cellular interactions within this biological system are not fully understood and need further insights. Thus, in this review, we summarize the essential roles of CCR7 and its receptors in breast cancer progression. Furthermore, we discuss the mechanisms of regulation that may lead to novel opportunities for therapeutic intervention. Despite the enormous advances in our knowledge of the nature of the chemokines in breast cancer metastasis, research about the involvement of CCR7 in cancer progression is still limited. Therefore, further studies are essential to illustrate the distinct roles of CCR7 in cancer progression and validate its potential as a preventive bio-factor for human breast cancer metastasis by targeting chemokine receptor genes.

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CC chemokine ligand 21 enhances the immunogenicity of the breast cancer cell line MCF-7 upon assistance of TLR2

Cited by 22 publications

References 28 publications

TLR2 enhances ovarian cancer stem cell self-renewal and promotes tumor repair and recurrence

TLR2 enhances ovarian cancer stem cell self-renewal and promotes tumor repair and recurrence

CC Chemokines in a Tumor: A Review of Pro-Cancer and Anti-Cancer Properties of Receptors CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10 Ligands

The Role of CCL21/CCR7 Chemokine Axis in Breast Cancer Progression

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