A systematic study of Girdin on cell proliferation, migration and angiogenesis in different breast cancer subtypes

Autor: Ming Zhang, Jiajun Zhang, Hong Chen, Zhigao Li, Hongbin Wang, Li Wei
Rok vydání: 2017
Předmět:
Vascular Endothelial Growth Factor A
0301 basic medicine
Cancer Research
Cell Survival
Angiogenesis
Vesicular Transport Proteins
Breast Neoplasms
Biology
Models
Biological
Biochemistry
Phosphatidylinositol 3-Kinases
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Breast cancer
Cell Movement
Cell Line
Tumor
Genetics
medicine
Humans
RNA
Small Interfering
skin and connective tissue diseases
Molecular Biology
Protein kinase B
Cell Proliferation
Neovascularization
Pathologic
Akt/PKB signaling pathway
Microfilament Proteins
Cancer
medicine.disease
Vascular endothelial growth factor
Vascular endothelial growth factor A
030104 developmental biology
Oncology
chemistry
Gene Knockdown Techniques
030220 oncology & carcinogenesis
Cancer cell
Cancer research
Molecular Medicine
Female
Proto-Oncogene Proteins c-akt
Zdroj: Molecular Medicine Reports. 16:3351-3356
ISSN: 1791-3004
1791-2997
Popis: Breast cancer has one of the highest incidences in females worldwide. Girdin is a novel actin‑binding protein, that induces cell migration and angiogenesis. However, a systematic study of Girdin function in distinct subtypes of breast cancer has not been reported to date. Therefore, the present study aimed to investigate the role of Girdin on cell proliferation, migration and angiogenesis in different subtypes of breast cancer. For this purpose, the breast epithelial MCF‑7, breast ductal T47D and breast metastatic MDA‑MB‑231 cancer cell lines were selected. Girdin small interfering RNA (siRNA) was transfected into MCF‑7, T47D and MDA‑MB‑231 cells. Girdin knockdown suppressed cell viability and migration in the different cancer cells tested. Girdin knockdown also suppressed mRNA expression of vascular endothelial growth factor (VEGF), and activation of phosphatidyl inositol 3‑kinase (PI3K) and RAC‑α serine/threonine‑protein kinase (Akt) in the subtypes tested. In conclusion, these data indicate that Girdin knockdown suppressed cell viability and migration and may suppress angiogenesis via the PI3K/Akt signaling pathway, in various breast cancers subtypes. The present study therefore suggests a role for Girdin as a novel therapeutic target for breast cancer, independent of subtype.
Databáze: OpenAIRE
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