The Crosstalk between Ovarian Cancer Stem Cell Niche and the Tumor Microenvironment

Abstract

Ovarian cancer is one of the most important causes of cancer-related death among women in the world. Despite advances in ovarian cancer treatment, 70–80% of women who initially respond to therapy eventually relapse and die. There is evidence that a small population of cells within the tumors called cancer stem cells (CSCs) could be responsible for treatment failure due to their enhanced chemoresistance and tumorigenicity. These cells reside in a niche that maintains the principal properties of CSCs. These properties are associated with the capacity of CSCs to interact with different cells of the tumor microenvironment including mesenchymal stem cells, endothelial cells, immune cells, and fibroblasts, promoting cancer progression. This interaction can be mediated by cytokines, growth factors, lipids, and/or extracellular vesicles released in the CSC niche. In this review, we will discuss how the interaction between ovarian CSCs and the tumor microenvironment can contribute to the maintenance of the CSC niche and consequently to tumor progression in ovarian cancer.

Investigation of Immune‐related Makers Associated with Tumor-infiltrating T Cells in Ovarian Cancer

“…OV is one of the most common oncogenic malignancies among women. Despite multiple progress in OV treatment, 70-80% of patients with OV who initially respond to treatment eventually relapse and die (32). Immunotherapy as a cancer treatment has become a growing eld, but reports of success in treating epithelial OV are limited (33).…”

Combination of Cisplatin-Withaferin Based on PEGylated Liposome Nanoparticles as Alternative Therapy for Ovarian Cancer

“…29 Penjelasan terkait kekambuhan pada kanker ovarium, erat kaitannya dengan pembawaan sifat resisten dan interaksi dengan tumor microenvironment. [35][36][37] Metastasis diinisiasi oleh CSC yang berdiferensiasi menjadi ovarian cancer stem cell (ovarian CSC) dan memroduksi Growth-regulated oncogene 1 (GRO-1) sehingga menginisiasi transformasi fibroblast menjadi senescent fibroblast. Senescent fibroblast memicu transformasi sel sehingga terjadi metastasis melalui pembentukan ephitelial-mesenchimal transition (EMT).…”

“…Selain itu, peningkatan ekspresi reseptor Notch1 menyebabkan peningkatan hairy/enhancer of split 1 (Hes 1) dan hes-related with YRPW motifs 1 (Hey1) yang berfungsi dalam pengaturan transkripsi gen yang terlibat dalam proses apoptosis (Gambar 1). 28 [32][33][34][35][36][37][38][39][40][41][42][43][44][45][46] Review Article salah satu metode penghantaran obat dengan wujud berupa vesikel artifisial yang berbentuk bulat. 48,49 Rongga dan membran fosfolipid bilayer yang terdapat pada liposom memungkinkan obat hidrofilik maupun hidrofobik terangkut di dalamnya.…”

Cancer stem cells and fibroblast niche cross talk in an in‐vitro oral dysplasia model

“…Further studies have correlated expression of CSC ( CD44, ALDH1A1, NOTCH1 ) and Epithelial Mesenchymal Transition (EMT) ( CADHERIN, TWIST, TGF‐βeta, MMPs) markers with the process of invasion and metastasis . Additionally, microenvironment is known to be a major player in maintaining CSC properties in different cancers . Factors released from cancer associated fibroblasts (CAF), such as chondroitin‐sulfate, proteoglycan‐serglycin, promotes tumor growth, invasion, migration and colonisation in breast and lung cancers in CD44‐dependent manner .…”

“…[13][14][15] Additionally, microenvironment is known to be a major player in maintaining CSC properties in different cancers. [16][17][18] Factors released from cancer associated fibroblasts (CAF), such as chondroitin-sulfate, proteoglycan-serglycin, promotes tumor growth, invasion, migration and colonisation in breast and lung cancers in CD44-dependent manner. 19 Co-culture of stromal cells such as omental adipose derived and/or bone-marrow mesenchymal stem cells with tumor associated macrophages have been correlated with aberrant expression of stem cell profile in ovarian, myeloma, breast, and gastric cancer cells.…”