Abstract
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 language | English |
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Number of pages | 331 |
ISBN (Electronic) | 9783030805586 |
DOIs | |
State | Published - Jan 1 2022 |
Bibliographical note
Publisher Copyright:© Springer Nature Switzerland AG 2021. All rights reserved.
Keywords
- 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