scholarly journals The Role of Cell Adhesion Molecule 1 (CADM1) in Cutaneous Malignancies

2020 ◽  
Vol 21 (24) ◽  
pp. 9732
Author(s):  
Yu Sawada ◽  
Emi Mashima ◽  
Natsuko Saito-Sasaki ◽  
Motonobu Nakamura
Keyword(s):  
Cell Adhesion ◽  
Cell Carcinoma ◽  
Adhesion Molecule ◽  
Immune Cells ◽  
Cell Adhesion Molecule ◽  
Tumor Development ◽  
Suppressor Gene ◽  
Cutaneous Lymphomas ◽  
Cell Adhesion Molecule 1

Cell adhesion ability is one of the components to establish cell organization and shows a great contribution to human body construction consisting of various types of cells mixture to orchestrate tissue specific function. The cell adhesion molecule 1 (CADM1) is a molecule of cell adhesion with multiple functions and has been identified as a tumor suppressor gene. CADM1 has multifunctions on the pathogenesis of malignancies, and other normal cells such as immune cells. However, little is known about the function of CADM1 on cutaneous cells and cutaneous malignancies. CADM1 plays an important role in connecting cells with each other, contacting cells to deliver their signal, and acting as a scaffolding molecule for other immune cells to develop their immune responses. A limited number of studies reveal the contribution of CADM1 on the development of cutaneous malignancies. Solid cutaneous malignancies, such as cutaneous squamous cell carcinoma and malignant melanoma, reduce their CADM1 expression to promote the invasion and metastasis of the tumor. On the contrary to these cutaneous solid tumors except for Merkel cell carcinoma, cutaneous lymphomas, such as adult-T cell leukemia/lymphoma, mycosis fungoides, and Sézary syndrome, increase their CADM1 expression for the development of tumor environment. Based on the role of CADM1 in the etiology of tumor development, the theory of CADM1 contribution will desirably be applied to skin tumors according to other organ malignancies, however, the characteristics of skin as a multicomponent peripheral organ should be kept in mind to conclude their prognoses.

scholarly journals Evolutionary conserved role of neural cell adhesion molecule-1 in memory

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Vanja Vukojevic ◽  
Pavlina Mastrandreas ◽  
Andreas Arnold ◽  
Fabian Peter ◽  
Iris-T. Kolassa ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Neural Cell ◽  
Neural Cell Adhesion ◽  
Cell Adhesion Molecule 1

scholarly journals Dual Role of Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 in Angiogenesis and Invasion of Human Urinary Bladder Cancer

2004 ◽  
Vol 64 (24) ◽  
pp. 8932-8938 ◽  
Author(s):  
Leticia Oliveira-Ferrer ◽  
Derya Tilki ◽  
Gudrun Ziegeler ◽  
Jessica Hauschild ◽  
Sonja Loges ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Adhesion ◽  
Urinary Bladder ◽  
Carcinoembryonic Antigen ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Urinary Bladder Cancer ◽  
Related Cell ◽  
Cell Adhesion Molecule 1

scholarly journals Antidiabetic DPP-4 Inhibitors Reprogram Tumor Microenvironment That Facilitates Murine Breast Cancer Metastasis Through Interaction With Cancer Cells via a ROS–NF-кB–NLRP3 Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Rui Li ◽  
Xin Zeng ◽  
Meihua Yang ◽  
Jinmei Feng ◽  
Xiaohui Xu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Tumor Microenvironment ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Diabetic Patients ◽  
Dipeptidyl Peptidase 4 Inhibitors ◽  
Cell Adhesion Molecule 1

Improvement of understanding of the safety profile and biological significance of antidiabetic agents in breast cancer (BC) progression may shed new light on minimizing the unexpected side effect of antidiabetic reagents in diabetic patients with BC. Our recent finding showed that Saxagliptin (Sax) and Sitagliptin (Sit), two common antidiabetic dipeptidyl peptidase-4 inhibitors (DPP-4i) compounds, promoted murine BC 4T1 metastasis via a ROS–NRF2–HO-1 axis in nonobese diabetic–severe combined immunodeficiency (NOD-SCID) mice. However, the potential role of DPP-4i in BC progression under immune-competent status remains largely unknown. Herein, we extended our investigation and revealed that Sax and Sit also accelerated murine BC 4T1 metastasis in orthotopic, syngeneic, and immune-competent BALB/c mice. Mechanically, we found that DPP-4i not only activated ROS–NRF2–HO-1 axis but also triggered reactive oxygen species (ROS)-dependent nuclear factor kappa B (NF-κB) activation and its downstream metastasis-associated gene levels in vitro and in vivo, while NF-кB inhibition significantly abrogated DPP-4i-driven BC metastasis in vitro. Meanwhile, inhibition of NRF2–HO-1 activation attenuated DPP-4i-driven NF-кB activation, while NRF2 activator ALA enhanced NF-кB activation, indicating an essential role of ROS–NRF2–HO-1 axis in DPP-4i-driven NF-кB activation. Furthermore, we also found that DPP-4i increased tumor-infiltrating CD45, MPO, F4/80, CD4, and Foxp3-positive cells and myeloid-derived suppressor cells (MDSCs), and decreased CD8-positive lymphocytes in metastatic sites, but did not significantly alter cell viability, apoptosis, differentiation, and suppressive activation of 4T1-induced splenic MDSCs. Moreover, we revealed that DPP-4i triggered ROS-NF-κB-dependent NLRP3 inflammasome activation in BC cells, leading to increase in inflammation cytokines such as interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), intercellular cell adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), IL-1β and IL-33, and MDSCs inductors granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF, and M-CSF, which play a crucial role in the remodeling of tumor immune-suppressive microenvironment. Thus, our findings suggest that antidiabetic DPP-4i reprograms tumor microenvironment that facilitates murine BC metastasis by interaction with BC cells via a ROS–NRF2–HO-1–NF-κB–NLRP3 axis. This finding not only provides a mechanistic insight into the oncogenic ROS–NRF2–HO-1 in DPP-4i-driven BC progression but also offers novel insights relevant for the improvement of tumor microenvironment to alleviate DPP-4i-induced BC metastasis.

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