E-Book 2nd Congress

  • The role of Entosis in cancer prognosis
  • Roqaye Karimi,1,* Alireza Soleimani,2 Mahin Behzadifard,3 Amir Atashi,4
    1. Department of Hematology and Cell Therapy, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
    2. Student Research Committee Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
    3. Dezful University of Medical Sciences, Dezful, Iran.
    4. Stem Cell and Tissue Engineering Research Center, Shahroud University of Medical Sciences, Shahroud, Iran.


  • Introduction: Recently, a novel type of programmed cell death occurring in cancer called entosis has been described, in which cancer cells engulf and kill their neighbors through a non-apoptotic mechanism involving autophagy and lysosome-mediated cell digestion, and benefit from their death, which is a mechanism whereby cells survive under stress and become more tumorigenic.
  • Methods: Cancerous tissues with increased number of entotic structures show a more malignant phenotype than the same variant without such structures. Therefore, entosis has the ability to promote tumor progression, as this process induces aneuploidy and polyploidy, and increases the intracellular nutrient pools to support the survival and proliferation of cancer cells and protect them from environmental factors such as chemotherapy or other adverse conditions caused by anticancer drugs. Such process can potentially facilitate the proliferation and metastasis of tumor cells and lead to chemotherapy failure or even cancer recurrence. Recently, it has been shown that resistance during tyrosine kinase inhibitor (TKI) nintedanib treatment in prostate cancer cells is induced through the activation of entosis.
  • Results: Entosis has been frequently identified in human malignancies, including lung, breast, stomach, liver, colon, and cervical cancers and melanoma, which are associated with poor prognosis. Several molecules and pathways are involved in the entosis process and induces entosis in human cancers, including cadherin proteins, E-cadherin or P-cadherin, and the Rho/Rho-associated kinase (ROCK) signaling pathway. On the other hand, TP53 and KRAS mutations increase the probability of cancer cells undergoing entosis. Interestingly, entosis has tumor suppressor activity and is able to induce cell death. There was only one case in which entotic structures were associated with reduced metastasis in pancreatic cancer, which is the opposite to other tumour types. Of course, it should be noted that the fate of entosis can be influenced by the interactions of cancer cell, tumor microenvironment and genetic factors.
  • Conclusion: All these findings open new perspectives to investigate entosis as a potential target for cancer therapy.
  • Keywords: Entosis, Cancer, Cancer prognosis