PDGF-D promotes cell growth, aggressiveness, angiogenesis and EMT transformation of colorectal cancer by activation of Notch1/Twist1 pathway

Chen, Jinhuang; Yuan, Wenzheng; Wu, Liang; Tang, Qiang; Xia, Qinghua; Ji, Jintong; Liu, Zhengyi; Ma, Zhuo; Zhou, Zili; Cheng, Yifeng; Shu, Xuefeng

doi:10.18632/oncotarget.14283

Cited by 65 publications

(55 citation statements)

References 21 publications

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“…Cells (SW480: 5 × 10 3 /200 μL, DLD1: 4 × 10 3 /200 μL and LoVo: 5 × 10 3 /200 μL) were seeded into a 96‐well plate. After 24, 48 and 72 hours, CCK8 assays were carried out to determine cell growth according to the manufacturer's protocol. The EDU assay was carried out using a Cell‐Light™ EDU Apollo ® 488 In Vitro Flow Cytometry Kit according to the manufacturer's protocol.…”

Section: Methodsmentioning

confidence: 99%

Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial‐mesenchymal transition and 5‐fluorouracil resistance

et al. 2018

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Nuclear factor I/B (NFIB) is a widely studied transcription factor that participates in tumor progression; nevertheless, studies on NFIB in colorectal cancer (CRC) are limited. In our study, Western blot and RT‐PCR analyses showed that NFIB was overexpressed in CRC tissues and cell lines, which was consistent with our bioinformatic analysis results. Furthermore, NFIB expression was closely related to the TNM stage of CRC. NFIB promoted cell proliferation and migration and inhibited cell apoptosis in vitro. Meanwhile, we discovered that NFIB accelerated xenograft tumor growth in vivo. In addition, NFIB weakened the sensitivity of CRC cells to 5‐fluorouracil (5‐FU). NFIB induced epithelial‐mesenchymal transition (EMT) by upregulating snail expression, which was accompanied by decreased E‐cadherin and Zo‐1 expression and increasedd Vimentin expression. Because the Akt pathway plays an important role in CRC progression, we examined whether there was a correlation between NFIB and the Akt pathway in cell proliferation and migration. Our results showed that NFIB promoted cell proliferation and increased 5‐FU resistance by activating the Akt pathway. In summary, our findings suggested that NFIB induced EMT of CRC cells via upregulating snail expression and promoted cell proliferation and 5‐FU resistance by activating the Akt pathway.

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Section: Methodsmentioning

confidence: 99%

Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial‐mesenchymal transition and 5‐fluorouracil resistance

et al. 2018

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“…The tumor-promoting activity of PDGFD has been reported for some PCa and CRC cell lines. (12,13) To determine the involvement of PDGFD in the proliferation of DU145, PC-3, DLD-1, and HCT116 cells, we carried out siRNA-mediated knockdown of PDGFD. PDGFD suppression decreased the reproductive ratios of all PCa and CRC cell lines tested (Fig.…”

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confidence: 99%

Identification of zinc finger protein of the cerebellum 5 as a survival factor of prostate and colorectal cancer cells

et al. 2017

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Identification of specific drug targets is very important for cancer therapy. We recently identified zinc finger protein of the cerebellum 5 (ZIC5) as a factor that promotes melanoma aggressiveness by platelet‐derived growth factor D (PDGFD) expression. However, its roles in other cancer types remain largely unknown. Here we determined the roles of ZIC5 in prostate cancer (PCa) and colorectal cancer (CRC) cells. Results showed that ZIC5 was highly expressed in CRC and dedifferentiated PCa tissues, whereas little expression was observed in relevant normal tissues. Knockdown of ZIC5 decreased proliferation of several PCa and CRC cell lines with induction of cell death. ZIC5 knockdown significantly suppressed PDGFD expression transcriptionally, and PDGFD suppression also decreased proliferation of PCa and CRC cell lines. In addition, suppression of ZIC5 or PDGFD expression decreased levels of phosphorylated focal adhesion kinase (FAK) and signal transducer and activator of transcription 3 (STAT3) which are associated with PCa and CRC aggressiveness. Furthermore, knockdown of ZIC5 or PDGFD enhanced death of PCa and CRC cells induced by the anti‐cancer drugs docetaxel or oxaliplatin, respectively. These results suggest that ZIC5 and PDGFD promote survival of PCa and CRC cells by enhancing FAK and STAT3 activity, and that the roles of ZIC5 are consistent across several cancer types.

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“…The signal is transduced into the cell to promote differentiation, migration and survival (Heldin et al, 1998, Heldin andWestermark, 1999). PDGF-D is the latest and the least studied member of the PDGFs, which functions by binding either to the PDGFR-αβ or the PDGFR-ββ (Figure 7) (Fredriksson et al, 2004) and seems to play a role in cancers such as breast cancer and CRC (Ahmad et al, 2011, Chen et al, 2016.…”

Section: Platelet-derived Growth Factor Dmentioning

confidence: 99%

“…PDGF-D is expressed in various types of cancers such as breast cancer and CRC (Ahmad et al, 2011, Chen et al, 2016 and is shown to be involved in the regulation of cellular processes important in cancer development (Ustach and Kim, 2005, Li et al, 2003, Chen et al, 2016. PDGF-D induces its cellular effects by binding to and activating the receptor PDGFR-β (Li et al, 2003, Wang et al, 2009), a tyrosine kinase receptor, which, due to its phosphorylation is able to trigger a number of signalling pathways also in CRC (Chen et al, 2016) and in the matched normal tissue, which was in line with a previous study (Chen et al, 2016). In the study by Chen et al the expression of PDGF-D was associated with clinicopathological features such as TNM stage, lymph node invasion, and tumour differentiation (Chen et al, 2016).…”

Section: Possible Role and Therapeutic Target Of Pdgf-d Signalling Inmentioning

confidence: 99%

“…PDGF-D induces its cellular effects by binding to and activating the receptor PDGFR-β (Li et al, 2003, Wang et al, 2009), a tyrosine kinase receptor, which, due to its phosphorylation is able to trigger a number of signalling pathways also in CRC (Chen et al, 2016) and in the matched normal tissue, which was in line with a previous study (Chen et al, 2016). In the study by Chen et al the expression of PDGF-D was associated with clinicopathological features such as TNM stage, lymph node invasion, and tumour differentiation (Chen et al, 2016). In this study the correlation between expression levels of PDGF-D and clinicopathological covariates was not investigated since no differences in tissue expression levels of the protein were observed by ELISA.…”

Section: Possible Role and Therapeutic Target Of Pdgf-d Signalling Inmentioning

confidence: 99%

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Circulating and genetic factors in colorectal cancer: Potential factors for establishing prognosis?

Olsen¹

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Colorectal cancer (CRC) is defined as a cancer appearing in the colon or in the rectum. In Sweden, ~ 6300 individuals were diagnosed with the disease in 2014 and ~ 2550 individuals diagnosed with CRC die each year due to their cancer. Surgery is the main treatment option of CRC and a survival rate of ~ 10 % is estimated if distant metastases have developed. It is therefore of importance to find factors that may be useful together with tumour, node, metastasis (TNM) stage to establish early CRC diagnosis, prognosis and follow-up of CRC patients. The aim of this thesis was to study the possible association of CD93, PLA2G4C, PDGF-D and inflammatory cytokines with CRC disease progression.In a prospective study approach CD93 and PLA2G4C single nucleotide polymorphisms (SNPs) were of potential importance in CRC prognosis.The T/T genotype of CD93 was associated with an increased CD93 expression in CRC tissue.Further, CRC patients carrying this genotype were associated with disseminated CRC at diagnosis and a lower recurrence-free survival after surgery. The A allele of a SNP of PLA2G4C was a stronger predictor for CRC-specific mortality than the conventional risk factors used in the clinic for selection of TNM stage II patients for adjuvant treatment. This indicates that the T/T genotype of CD93 and the A allele of PLA2G4C may be potential genetic factors related to disease severity and spread. Furthermore, they distinguish CRC patients that may benefit from a more comprehensive follow-up and adjuvant treatment.To study the putative involvement of PDGF-D in CRC the effects of PDGF-D signalling was studied in vitro. PDGF-D signalling altered the expression of genes of importance in CRC carcinogenesis and proliferation which was blocked by imatinib, a tyrosine kinase inhibitor.This indicates that PDGF-D signalling may be an important pathway in CRC progression and a potential target in CRC treatment.vi The analysis of various inflammatory cytokines in plasma at diagnosis showed an association between high levels and increased total-or CRC-specific mortality two years after surgery.High levels of CCL1 and CCL24 was the only cytokines strongly correlated with a worse CRC prognosis after statistical adjustments and may be of interest for further evaluation.In conclusion, this thesis presents circulating and genetic factors such as CD93, PLA2G4C, PDGF-D, CCL1 and CCL24 that may be of importance in CRC progression and may be of clinical value together with TNM stage in establishing prognosis. III.Olsen RS, Dimberg J, Geffers R, Wågsäter D. Possible role and therapeutic target of

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PDGF-D promotes cell growth, aggressiveness, angiogenesis and EMT transformation of colorectal cancer by activation of Notch1/Twist1 pathway

Cited by 65 publications

References 21 publications

Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial‐mesenchymal transition and 5‐fluorouracil resistance

Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial‐mesenchymal transition and 5‐fluorouracil resistance

Identification of zinc finger protein of the cerebellum 5 as a survival factor of prostate and colorectal cancer cells

Circulating and genetic factors in colorectal cancer: Potential factors for establishing prognosis?

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