Role of SPARC in the epithelial-mesenchymal transition induced by PTHrP in human colon cancer cells

Autor: María Belén Novoa Díaz, Claudia Gentili, Exequiel Alonso, María José Torres, Natalia Calvo, Héctor R. Contreras, Alexander Herrera, Fernanda López-Moncada, Pedro Carriere, Norberto Ariel Gandini, Graciela Gigola
Rok vydání: 2021
Předmět:
musculoskeletal diseases
0301 basic medicine
Colorectal cancer
030209 endocrinology & metabolism
Biochemistry
Cell Line
Mice
03 medical and health sciences
0302 clinical medicine
Endocrinology
Antigens
CD
Cell Movement
In vivo
Tumor Microenvironment
medicine
Animals
Humans
Osteonectin
Epithelial–mesenchymal transition
neoplasms
Molecular Biology
Cell Proliferation
Tumor microenvironment
Transition (genetics)
Chemistry
Parathyroid Hormone-Related Protein
Endothelial Cells
Cell migration
Cadherins
HCT116 Cells
musculoskeletal system
medicine.disease
digestive system diseases
Up-Regulation
Gene Expression Regulation
Neoplastic
Human colon cancer
On cells
030104 developmental biology
Culture Media
Conditioned
Colonic Neoplasms
Disease Progression
Cancer research
Caco-2 Cells
Neoplasm Transplantation
hormones
hormone substitutes
and hormone antagonists
Zdroj: Molecular and Cellular Endocrinology. 530:111253
ISSN: 0303-7207
DOI: 10.1016/j.mce.2021.111253
Popis: Parathyroid hormone-related peptide (PTHrP) exerts its effects on cells derived from colorectal cancer (CRC) and tumor microenvironment and is involved in processes requiring the epithelial-mesenchymal transition (EMT). Here, we report that PTHrP modulates factors expression and morphological changes associated with EMT in HCT116 cells from CRC. PTHrP increased the protein expression of SPARC, a factor involved in EMT, in HCT116 cells but not in Caco-2 cells also from CRC but with less aggressiveness. PTHrP also increased SPARC expression and its subsequent release from endothelial HMEC-1 cells. The conditioned media of PTHrP-treated HMEC-1 cells induced early changes related to EMT in HCT116 cells. Moreover, SPARC treatment on HCT116 cells potentiated PTHrP modulation in E-cadherin expression and cell migration. In vivo PTHrP also increased SPARC expression and decreased E-cadherin expression. These results suggest a novel PTHrP action on CRC progression involving the microenvironment in the modulation of events associated with EMT.
Databáze: OpenAIRE
Externí odkaz: