Related Experiment Video
Updated: Mar 21, 2026

A Proximal Culture Method to Study Paracrine Signaling Between Cells
Published on: August 28, 2018
Tumor microenvironment: The culprit for ovarian cancer metastasis?
Zhongyue Luo1, Qiu Wang2, Wayne Bond Lau3
1Department of Obstetrics and Gynecology, Key Laboratory of Obstetrics & Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education, West China Second Hospital and The State Key Laboratory of Biotherapy/Collaborative Innovation Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Abstract:
Despite chemotherapy and surgical debulking options, ovarian cancer recurs and disseminates frequently, with poor prognosis. However, the molecular mechanisms underlying ovarian cancer metastasis still remain unelucidated. The tumor microenvironment, consisting of stromal cells (including fibroblasts, macrophages, regulatory T cells, myeloid-derived suppressor cells, endothelial cells, pericytes and platelets), the extracellular matrix component (EMC) (including inflammatory cytokines, chemokines, matrix metalloproteinases, integrins, and other secreted molecules) and exosomes (small extracellular vesicles loaded with molecules), establishes an autocrine-paracrine communication circuit that reinforces invasion and cancer cell metastasis via reciprocal signaling. Recent evidences have unraveled the significant contribution of tumor microenvironment to ovarian cancer metastasis. In this review, we provide a comprehensive landscape of the reciprocity between tumor stroma and ovarian cancer cells upon metastasis, aiming to offer novel clues on the development of novel diagnostic biomarkers and therapeutic targets for ovarian cancer in future clinical practice.
Insights
Ovarian cancer metastasis is driven by complex interactions within the tumor microenvironment. Understanding these signals between cancer cells and stroma can reveal new diagnostic and therapeutic targets.
Area of Science:
- Oncology
- Cancer Biology
- Molecular Mechanisms
Background:
- Ovarian cancer frequently recurs and disseminates despite current treatments, with poor patient prognosis.
- The molecular underpinnings of ovarian cancer metastasis remain incompletely understood.
- The tumor microenvironment (TME) plays a critical role in cancer progression.
Purpose of the Study:
- To comprehensively review the reciprocal signaling between ovarian cancer cells and the tumor stroma.
- To elucidate the molecular mechanisms driving ovarian cancer metastasis via the TME.
- To identify potential diagnostic biomarkers and therapeutic targets for ovarian cancer.
Main Methods:
- Literature review of recent evidence on tumor microenvironment and ovarian cancer metastasis.
- Analysis of the components of the tumor microenvironment, including stromal cells, extracellular matrix, and exosomes.
- Examination of the autocrine-paracrine communication circuits within the TME.
Main Results:
- The tumor microenvironment, comprising stromal cells, extracellular matrix, and exosomes, establishes communication circuits that promote ovarian cancer invasion and metastasis.
- Reciprocal signaling between tumor stroma and ovarian cancer cells is a significant contributor to metastasis.
- Specific components like inflammatory cytokines, chemokines, and matrix metalloproteinases are implicated in facilitating metastasis.
Conclusions:
- The tumor microenvironment is a key driver of ovarian cancer metastasis.
- Understanding the intricate signaling networks within the TME is crucial for developing effective treatments.
- This review provides insights for novel diagnostic biomarkers and therapeutic strategies for ovarian cancer.
More Related Videos
Related Concept Videos
The Tumor Microenvironment
The Tumor Microenvironment
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Mitogens and the Cell Cycle

