Platelet-derived growth factor-C functions as a growth factor in mouse embryonic stem cells and human fibrosarcoma cells

Tomoaki Kinjo,Takako Ikegami,Hiroshi Koide,Tadayuki Akagi,Takashi Yokota,Yuhki Tada,Chuanhai Sun,Tomomi Ikeda

doi:10.1186/s11658-018-0075-3

Abstract

BackgroundPlatelet-derived growth factor-C (PDGF-C) has been shown to be involved in several biological processes, such as embryonic development, wound healing and angiogenesis, as well as in diseases including tumor formation and fibrotic diseases. However, its role in fibrosarcoma and embryonic stem (ES) cells has not been elucidated.MethodsThe expression level of PDGF-C was measured using RT-PCR. The activity of PDGF-C was suppressed using RNA interference or a neutralizing antibody and the effect on cell growth was examined using the WST and soft agar assays.ResultsIn the tumor cell lines studied, the highest level of PDGF-C expression was in human HT1080 fibrosarcoma cells. In ES cells, it was highly expressed in the self-renewal state but not in the differentiated state. PDGF-C knockdown suppressed anchorage-dependent and -independent growth of HT1080 and ES cells. In addition, the suppression of PDGF-C activity by a neutralizing antibody retarded ES cell growth.ConclusionOur results suggest that PDGF-C plays an important role in the proliferation of fibrosarcoma and ES cells.

Highlights

Platelet-derived growth factor-C (PDGF-C) has been shown to be involved in several biological processes, such as embryonic development, wound healing and angiogenesis, as well as in diseases including tumor formation and fibrotic diseases
PDGF-C is highly expressed in HT1080 cells We examined the expression level of PDGF-C in the HT1080 fibrosarcoma cell line
PDGF-C is required for anchorage-dependent and -independent HT1080 cell growth We examined the requirement of PDGF-C for cell growth in HT1080 cells through knockdown experiments with artificial micro RNA against PDGF-C

Summary

Introduction

Platelet-derived growth factor-C (PDGF-C) has been shown to be involved in several biological processes, such as embryonic development, wound healing and angiogenesis, as well as in diseases including tumor formation and fibrotic diseases. Several transcription factors, including Oct3/4 and STAT3, play important roles in the self-renewal of ES cells by forming transcription factor networks to stimulate the expression of a set of genes that promote self-renewal in ES cells [1]. ES cells share many biological properties with cancer cells [2]. Both ES and cancer cells can survive and grow in the absence of anchorage, and produce tumors when injected into nude mice. Several oncogenic pathways, including the STAT3 and Wnt/β-catenin pathways, play important roles in ES cell self-renewal [3,4,5,6,7,8]. There is an overlap in the expression of certain genes in ES and cancer cells [9]

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Conclusion