Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines

Lirdprapamongkol, Kriengsak; Chiablaem, Khajeelak; Sila-asna, Monnipha; Surarit, Rudee; Bunyaratvej, Ahnond; Svasti, Jisnuson

doi:10.1016/j.bbrc.2012.05.009

Cited by 35 publications

(25 citation statements)

References 29 publications

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“…As a result, the idea of a special blood supply called vasculogenic mimicry (VM) was put forth. VM was later discovered in various types of solid tumors, especially in highly malignant solid tumors (Lin et al, 2012;Lirdprapamongkol et al, 2012;Tijeras-Raballand et al, 2014). In this study, HE stain-ing also showed tubular structures composed of tumor cells with erythrocytes inside parts of the lumens.…”

Section: Discussionsupporting

confidence: 63%

Vasculogenic mimicry and hypoxia-inducible factor-1α expression in cervical squamous cell carcinoma

Zhou¹,

Huang²,

Gong³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. In this study, the existence of vasculogenic mimicry (VM) in cervical squamous cell carcinoma was investigated. To this end, the relationship between hypoxia-inducible factor 1α (HIF-1α) and the development, infiltration, and metastasis of cervical squamous cell carcinoma was studied. Between January 2010 and December 2010, 67 human cervical squamous carcinoma tissue samples were collected and stained by CD34/periodic acid-Schiff double staining to detect the existence of VM. HIF-1α expression was analyzed by immunohistochemistry. The relationship between VM and HIF-1α was also analyzed. Normal cervical tissues (20 cases) from patients who had uterine surgeries in the same period were collected as controls. In the cervical squamous carcinoma tissues, positive rates of VM and HIF-1α were 38.81% (26/67) and 64.18% (43/67), respectively. This was significantly higher than those in the normal cervical tissues [0 (0/20); P < 0.05]. VM rates in cervical squamous carcinoma tissues from patients with different pathological grades, Federation of Gynecology and Obstetrics (FIGO) stages, and lymph node metastasis states were also significantly different (P < 0.05). In addition, significant differences in HIF-1α positivity rates were observed among patients with varying tumor sizes and lymph node metastasis states (P < 0.05). Positive correlation was found between VM and HIF-1α (r = 0.339, P < 0.05). To summarize, we found VM in cervical squamous carcinoma; high expression of HIF-1α may promote VM formation, as well as cervical squamous cell infiltration and metastasis.

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Section: Discussionsupporting

confidence: 63%

Vasculogenic mimicry and hypoxia-inducible factor-1α expression in cervical squamous cell carcinoma

Zhou¹,

Huang²,

Gong³

et al. 2016

Genet. Mol. Res.

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“…RNA extraction and first-strand cDNA synthesis were performed as previously described (20). Real-time PCR was run on a LightCycler ® 2.0 Instrument (Roche), using QuantiTect™ SYBR Green PCR Master mix (Qiagen, Valencia, CA, USA).…”

Section: Quantitative Reverse Transcriptase-polymerase Chain Reactionmentioning

confidence: 99%

A flavonoid chrysin suppresses hypoxic survival and metastatic growth of mouse breast cancer cells

et al. 2013

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Abstract. Tumor hypoxia commonly occurs in solid tumors, and correlates with metastasis. Current cancer therapies are inefficient in curing metastatic disease. Herein, we examined effect of Thai propolis extract and its major constituent, chrysin, on hypoxic survival of 4T1 mouse breast cancer cells in vitro, and investigated its underlying mechanism. In vivo effect of chrysin on metastatic progression of cancer cells was studied, both as a single agent and in combination with another antimetastatic agent, agonistic monoclonal antibody targeting the DR5 TRAIL receptor (DR5 mAb). Thai propolis extract and chrysin decreased survival of 4T1 cells after exposure to hypoxia (1% O 2 ), for 2 days. Immunoblot analysis revealed that chrysin inhibited hypoxia-induced STAT3 phosphorylation without affecting HIF-1α protein level. Chrysin also abrogated hypoxia-induced VEGF gene expression as determined by qRT-PCR. The in vivo effect of chrysin was determined in a spontaneous metastasis mouse model of breast cancer, either alone or in combination with DR5 mAb. Daily oral administration of chrysin in Balb/c mice implanted with 4T1 cells significantly suppressed growth of lung metastatic colonies. Moreover, antimetastatic activity of DR5 mAb was enhanced when given in combination with chrysin. We demonstrate that chrysin has potential in controlling metastatic progression.

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“…Considering the phenomenon that tumour cells are able to transdifferentiate into endothelium-like cells which are mesenchymal cells, it can be demonstrated that epithelialmesenchymal transition (EMT) is vital in VM formation and tumour progression. However, the up-regulation of EMT-associated transcription factors can also contribute in VM-forming process [2][3][4]. The purpose of this article is to explore the most recent research in the relationship of EMT and VM and their corresponding mechanisms in tumorigenesis effect.…”

Section: Introductionmentioning

confidence: 99%

The relationship between vasculogenic mimicry and epithelial‐mesenchymal transitions

Liu

Qiao

Liang

et al. 2016

J Cellular Molecular Medi

101

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Vasculogenic mimicry ( VM ) is a vascular‐like structure which can mimic the embryonic vascular network pattern to nourish the tumour tissue. As a unique perfusion way, VM is correlated with tumour progression, invasion, metastasis and lower 5‐year survival rate. Notably, epithelial‐mesenchymal transition ( EMT ) regulators and EMT ‐related transcription factors are highly up‐regulated in VM ‐forming tumour cells, which demonstrated that EMT may play a crucial role in VM formation. Therefore, the up‐regulation of EMT ‐associated adhesion molecules and other factors can also make a contribution in VM ‐forming process. Depending on these discoveries, VM and EMT can be utilized as therapeutic target strategies for anticancer therapy. The purpose of this article is to explore the advance research in the relationship of EMT and VM and their corresponding mechanisms in tumorigenesis effect.

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Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines

Cited by 35 publications

References 29 publications

Vasculogenic mimicry and hypoxia-inducible factor-1α expression in cervical squamous cell carcinoma

Vasculogenic mimicry and hypoxia-inducible factor-1α expression in cervical squamous cell carcinoma

A flavonoid chrysin suppresses hypoxic survival and metastatic growth of mouse breast cancer cells

The relationship between vasculogenic mimicry and epithelial‐mesenchymal transitions

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