Par-4 is a naturally occurring tumor suppressor. Studies have indicated that overexpression of Par-4 selectively induces apoptosis in cancer cells while leaving normal, health, cells unaffected. Mechanisms contributing to this cancer-selective action of Par-4 have been associated with PKA activation of intracellular Par-4 in cancer cells or GRP78 expression primarily on the surface of cancer cells. On the other hand, endogenous Par-4 sensitizes cells to the action of a broad range of apoptotic inducers acting via the extrinsic and intrinsic pathways. A number of binding partners of Par-4 have been identified and shown to regulate Par-4 function in cancer and other diseases, such as Alzheimer's and major depression. Recent studies have recognized a number of natural products, dietary supplements, synthetic molecules and FDA-approved drugs that induce the secretion of Par-4 protein to cause apoptosis in primary or metastatic tumors, one of which is in clinical trials. More than 50 different laboratories worldwide are involved in Par-4 based research of this unique protein that has progressed from the bench to clinical trials. This second, companion volume will provide a comprehensive overview of Par-4's role in cancer and other diseases. Chapters are written by leading researchers, and will be useful for a broad audience across the scientific community, particularly students and trainees, who are the next generation of scientists and clinicians to participate in new studies and discoveries on Par-4.

Original languageEnglish
Number of pages331
ISBN (Electronic)9783030805586
StatePublished - Jan 1 2022

Bibliographical note

Publisher Copyright:
© Springer Nature Switzerland AG 2021. All rights reserved.


  • Breast cancer
  • CLL
  • Cardiac fibroblast senescence
  • Dopamine signaling
  • Endometrial cancer
  • GI tumors
  • Glioblastoma
  • Lung cancer
  • Major depression
  • Nasopharyngeal carcinoma
  • Ocular development
  • Ovarian cancer
  • Pancreatic cancer
  • Prostate cancer
  • Protein expression
  • SAC
  • TCL1
  • THAP
  • TNF
  • Type 2 diabetes

ASJC Scopus subject areas

  • General Medicine


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