The paracrine induction of prostate cancer progression by caveolin-1
Journal
Cell Death and Disease
Journal Volume
10
Journal Issue
11
Date Issued
2019
Author(s)
Lin, C.-J.
Yun, E.-J.
Lo, U.-G.
Tai, Y.-L.
Deng, S.
Hernandez, E.
Dang, A.
Chen, Y.-A.
Saha, D.
Mu, P.
Lin, H.
Shen, T.-L.
Lai, C.-H.
Abstract
A subpopulation of cancer stem cells (CSCs) plays a critical role of cancer progression, recurrence, and therapeutic resistance. Many studies have indicated that castration-resistant prostate cancer (CRPC) is associated with stem cell phenotypes, which could further promote neuroendocrine transdifferentiation. Although only a small subset of genetically pre-programmed cells in each organ has stem cell capability, CSCs appear to be inducible among a heterogeneous cancer cell population. However, the inductive mechanism(s) leading to the emergence of these CSCs are not fully understood in CRPC. Tumor cells actively produce, release, and utilize exosomes to promote cancer development and metastasis, cancer immune evasion as well as chemotherapeutic resistance; the impact of tumor-derived exosomes (TDE) and its cargo on prostate cancer (PCa) development is still unclear. In this study, we demonstrate that the presence of Cav-1 in TDE acts as a potent driver to induce CSC phenotypes and epithelial–mesenchymal transition in PCa undergoing neuroendocrine differentiation through NFκB signaling pathway. Furthermore, Cav-1 in mCRPC-derived exosomes is capable of inducing radio- and chemo-resistance in recipient cells. Collectively, these data support Cav-1 as a critical driver for mCRPC progression. ? 2019, This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply. This article is published with open access).
SDGs
Other Subjects
caveolin 1; CD24 antigen; Hermes antigen; immunoglobulin enhancer binding protein; messenger RNA; protein p53; protein ZO1; retinoblastoma protein; uvomorulin; vimentin; CAV1 protein, human; caveolin 1; tumor protein; Article; cancer growth; cancer resistance; cancer stem cell; castration resistant prostate cancer; cell differentiation; cell invasion; cell migration; cell survival; controlled study; epithelial mesenchymal transition; exosome; human; human cell; immune evasion; liquid biopsy; male; metastasis; paracrine signaling; primary tumor; priority journal; prostate cancer; radiosensitivity; signal transduction; animal; metabolism; mouse; pathology; SCID mouse; signal transduction; tumor cell line; Animals; Caveolin 1; Cell Line, Tumor; Exosomes; Humans; Male; Mice; Mice, SCID; Neoplasm Proteins; Paracrine Communication; Prostatic Neoplasms, Castration-Resistant; Signal Transduction
Publisher
Nature Publishing Group
Type
journal article