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A Proximal Culture Method to Study Paracrine Signaling Between Cells

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Published on: August 28, 2018

Extracellular Signaling Molecules from Adipose-Derived Stem Cells and Ovarian Cancer Cells Induce a Hybrid

Vinícius Augusto Simão¹, Juliana Ferreira Floriano², Roberta Carvalho Cesário¹

¹Department of Structural and Functional Biology, Institute of Biosciences, São Paulo State University (Unesp), Botucatu 18618-689, São Paulo, Brazil.

|March 12, 2025

Summary

This summary is machine-generated.

Extracellular vesicles and secreted molecules from stem cells and ovarian cancer cells promote tumor growth and metastasis. Targeting these interactions may offer new therapeutic strategies for ovarian cancer.

Keywords:

OVCAR3 SKOV3 adipose-derived mesenchymal stem cells cell invasion and migration conditioned medium exosome indirect co-culture metastable phenotype secretome small extracellular vesicles

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Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation

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Published on: August 23, 2018

Area of Science:

Oncology
Cell Biology
Biochemistry

Background:

Ovarian cancer (OC) presents high mortality due to late diagnosis and metastasis.
Adipose-derived mesenchymal stem cells (ASCs) and OC cells interact through secreted factors.

Purpose of the Study:

To investigate the role of extracellular signaling molecules from ASCs and OC cells in OC progression.
To elucidate the impact of small extracellular vesicles (sEVs) and conditioned medium (CM) on OC cell behavior and phenotype.

Main Methods:

Analysis of conditioned medium (CM) and small extracellular vesicles (sEVs) secreted by ASCs and OC cells.
Assessment of OC cell colony formation, invasion, and migration.
Evaluation of signaling pathways (TGFβ/Smad, p38MAPK/ERK1/2, Wnt/β-catenin, MMP-9) and protein expression (E-cadherin, Snail/Slug).
In silico analysis of patient data.

Main Results:

ASC-derived sEVs/CM promoted OC cell growth, invasion, and migration, upregulating key signaling pathways.
OC-derived sEVs/CM induced a pro-tumorigenic phenotype in ASCs.
Both cell types showed increased expression of E-cadherin and Snail/Slug, indicating enhanced plasticity and metastatic potential.
Tumor-supportive molecules (TNF-α, Tenascin-C, MMP-2, SDF-1α) were identified in the secretome.
In silico analysis correlated these molecular changes with poor OC prognosis.

Conclusions:

Bidirectional communication via sEVs and secretomes critically drives OC progression and metastasis.
These interactions influence cellular plasticity and phenotypic transitions, contributing to poor outcomes.
Targeting EV-mediated communication presents a promising therapeutic avenue for ovarian cancer.