Autophagy promotes the survival and development of tumors by participating in the formation of vasculogenic mimicry

  • Authors:
    • Yun-Peng Ding
    • Xiao-Dong Yang
    • Yong Wu
    • Chun-Gen Xing
  • View Affiliations

  • Published online on: March 12, 2014     https://doi.org/10.3892/or.2014.3087
  • Pages: 2321-2327
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Autophagy, type II nonapoptotic cell death, is characterized by the formation of double-membrane cytosolic vesicles, the recycling of damaged cytoplasmic content and the maintenance of genetic stability and cellular homeostasis, under conditions of nutrient starvation, hypoxia or other therapeutic stress. In the present study, we comprehensively discuss its indispensable role in the formation of vasculogenic mimicry (VM), capillary-like tubes consisting of cells from the tumor itself instead of vascular endothelial cells. A short hairpin RNA (shRNA) to silence beclin1, an autophagy-specific gene, was designed, synthesized and subcloned into a vector to establish an autophagy-inhibited group, while negative control and blank groups were also established using human gastric cancer SGC7901 cells. We then investigated the VM formation ability of these three groups and detected changes in gene expression, survival and invasion correspondingly. The results showed that, following the formation of VM, the expression of pluripotent genes (c-myc, oct3/4, sox-2) and autophagy-specific genes (beclin1, ATG5, ATG7) were increased, which was consistent with the negative control cell group. However, the autophagy inhibited cell group did not form VM, and the expression of pluripotent genes was decreased. Moreover, the inhibition of autophagy reduced the survival and invasive ability of cancer cells under stress. We suggest that during the formation of VM, the stable expression of genes and the maintenance of survival and invasion are indispensable. Under a stress environment, autophagy is activated to maintain the stability of gene expression, maintain survival and invasive ability and facilitate VM formation, which can provide nutrients, oxygen and invasive channels to tumors, facilitating survival and development under stress.
View Figures
View References

Related Articles

Journal Cover

May-2014
Volume 31 Issue 5

Print ISSN: 1021-335X
Online ISSN:1791-2431

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Ding Y, Yang X, Wu Y and Xing C: Autophagy promotes the survival and development of tumors by participating in the formation of vasculogenic mimicry. Oncol Rep 31: 2321-2327, 2014
APA
Ding, Y., Yang, X., Wu, Y., & Xing, C. (2014). Autophagy promotes the survival and development of tumors by participating in the formation of vasculogenic mimicry. Oncology Reports, 31, 2321-2327. https://doi.org/10.3892/or.2014.3087
MLA
Ding, Y., Yang, X., Wu, Y., Xing, C."Autophagy promotes the survival and development of tumors by participating in the formation of vasculogenic mimicry". Oncology Reports 31.5 (2014): 2321-2327.
Chicago
Ding, Y., Yang, X., Wu, Y., Xing, C."Autophagy promotes the survival and development of tumors by participating in the formation of vasculogenic mimicry". Oncology Reports 31, no. 5 (2014): 2321-2327. https://doi.org/10.3892/or.2014.3087