Promotion of tumor cell metastasis and vasculogenic mimicry by way of transcription coactivation by Bcl-2 and Twist1: A study of hepatocellular carcinoma

Sun, Tao; Sun, Bei; Zhao, Xuyao; Zhao, Nan; Dong, Xue; Che, Na; Yao, Zhi; Mei, Yue; Gu, Qing; Zong, Wen Kang; Liu, Zhi Yong

doi:10.1002/hep.24543

Cited by 140 publications

(133 citation statements)

References 33 publications

(38 reference statements)

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“…Bcl-2 exhibits an increased expression similar with Twist1 in hypoxia condition [29]. This phenomenon indicated that Bcl-2 and Twist1 possibly acted during the stress phase in the same cell and followed similar kinetics.…”

Section: Twist1/bmi1mentioning

confidence: 66%

The relationship between vasculogenic mimicry and epithelial‐mesenchymal transitions

Liu

Qiao

Liang

et al. 2016

J Cellular Molecular Medi

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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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Section: Twist1/bmi1mentioning

confidence: 66%

The relationship between vasculogenic mimicry and epithelial‐mesenchymal transitions

Liu

Qiao

Liang

et al. 2016

J Cellular Molecular Medi

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“…In addition to identification in invasive melanoma, VM has also been observed in other malignant solid tumors, including prostatic tumors (18,19), Ewing sarcoma (20), hepatocellular carcinoma (21,22), colorectal carcinoma (23) and glioma (24). Our previous study demonstrated that VM exists in glioblastomas and is a significant prognostic factor for patient survival (5).…”

Section: Discussionmentioning

confidence: 95%

Mammalian target of rapamycin signaling is involved in the vasculogenic mimicry of glioma via hypoxia-inducible factor-1α

Min

Sun

et al. 2014

Oncology Reports

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Abstract. The mammalian target of rapamycin (mTOR) is a crucial regulator in malignant gliomas. Vasculogenic mimicry (VM) describes functional channels established by highly malignant tumor cells that is different from endothelium-lined blood vessels. Our previous studies confirmed the existence and clinical significance of VM in medulloblastoma and glioblastoma. In the present study, by immunohistochemical and CD34/PAS histochemical double-staining, 34 cases (26.8%) with VM structures were identified among a total of 127 glioma cases, and these VM structures were associated with mTOR expression in the glioma specimens. In vitro, U87 malignant glioblastoma cells formed tube structures similar to HUVECs on Matrigel in 3D culture, and mTOR-specific inhibitor rapamycin inhibited VM formation in the U87 malignant glioblastoma cells under both normoxia and hypoxia. In addition, rapamycin and mTOR siRNA inhibited molecules in the signaling cascade of VM formation, particularly HIF-1α. Taken together, our results demonstrated that mTOR signaling is involved in VM formation, and may be a potential therapeutic target for gliomas.

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“…To our knowledge, this is the first report demonstrating that the prosurvival Bcl-2 proteins are direct targets of the p53/p21 complex. In addition to cell invasion and death, prosurvival Bcl-2 proteins can regulate various other cellular functions, including autophagy (24)(25)(26)(27), senescence (28)(29)(30), and the epithelial-mesenchymal transition (31)(32)(33)(34). Notably, these cellular functions are also regulated by p53 and p21 (1,2,30,(35)(36)(37)(38)(39).…”

Section: Discussionmentioning

confidence: 99%

The p53/p21 Complex Regulates Cancer Cell Invasion and Apoptosis by Targeting Bcl-2 Family Proteins

et al. 2017

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The tumor suppressor p53 binds prosurvival Bcl-2 family proteins such as Bcl-w and Bcl-X L to liberate Bax, which in turn exerts proapoptotic or anti-invasive functions depending on stress context. On the basis of our previous finding that p53 interacts with p21, we investigated the possible involvement of p21 in these functions. Here, we report that although p53 can bind Bcl-w alone, it requires p21 to liberate Bax to suppress cell invasion and promote cell death. p21 bound Bcl-w, forming a p53/p21/Bcl-w complex in a manner that maintained all pairwise p53/p21, p21/Bcl-w, and p53/Bcl-w interactions. This allowed Bax liberation from the complex. Accordingly, a p53 derivative incapable of binding p21 failed to mediate radiotherapy-induced tumor cell death in mice. Bcl-X L also served as a target of the cooperative action of p53 and p21. Overall, our findings indicate that the p53/p21 complex rather than p53 itself regulates cell invasion and death by targeting Bcl-2 proteins. We propose that the p53/p21 complex is a functional unit that acts on multiple cell components, providing a new foundation for understanding the tumor-suppressing functions of p53 and p21. Cancer Res; 77(11); 3092-100. Ó2017 AACR.

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Promotion of tumor cell metastasis and vasculogenic mimicry by way of transcription coactivation by Bcl-2 and Twist1: A study of hepatocellular carcinoma

Cited by 140 publications

References 33 publications

The relationship between vasculogenic mimicry and epithelial‐mesenchymal transitions

The relationship between vasculogenic mimicry and epithelial‐mesenchymal transitions

Mammalian target of rapamycin signaling is involved in the vasculogenic mimicry of glioma via hypoxia-inducible factor-1α

The p53/p21 Complex Regulates Cancer Cell Invasion and Apoptosis by Targeting Bcl-2 Family Proteins

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