Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9

Jiang,Bin; Chen,Jinhuang; Yuan,Wenzheng; Ji,Jintong; Liu,Zhengyi; Wu,Liang; Tang,Qiang; Shu,Xiaogang

doi:10.3892/ol.2017.7510

Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9

Authors:
- Bin Jiang
- Jinhuang Chen
- Wenzheng Yuan
- Jintong Ji
- Zhengyi Liu
- Liang Wu
- Qiang Tang
- Xiaogang Shu
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Affiliations: Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China
Published online on: December 5, 2017 https://doi.org/10.3892/ol.2017.7510
Pages: 1573-1579
Copyright: © Jiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Colorectal cancer (CRC) has been one of the most common types of cancer for decades worldwide. The pathogenesis of CRC is associated with the processes of activating oncogenes and inactivating anti‑oncogenes. Platelet‑derived growth factor‑D (PDGF‑D) was confirmed to regulate migration, invasion, proliferation, apoptosis and metastasis in various cancer cells. Overexpression of PDGF‑D exists in a number of human malignancies, including pancreatic, prostate and breast cancer. However, the expression and function of PDGF‑D and its associated molecular mechanism in CRC remain unclear. Thus, the expression of PDGF‑D was detected in CRC tissues and human colon cancer lines. Subsequently, the effects of PDGF‑D on the invasion, migration and proliferation of cancer cells were investigated. The corresponding molecular mechanism had also been explored. The present study revealed that PDGF‑D was upregulated not only in CRC tissues but also in CRC cell lines, and simultaneously, facilitated the processes of migration, invasion and proliferation. Silencing PDGF‑D in the SW480 cell line inhibited migration, invasion and proliferation distinctly, with reduced expression of Notch1 and matrix metalloproteinase‑9. Furthermore, upregulating PDGF‑D in HCT116 cells led to the opposite results. These findings indicate that PDGF‑D may be developed into a potential therapeutic target for CRC treatment.

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