Stem Cells as Target for Prostate cancer Therapy: Opportunities and Challenges
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Cancer stem cells (CSCs) and cells in a cancer stem cell-like (CSCL) state have proven to be responsible for tumor initiation, growth, and relapse in Prostate Cancer (PCa) and other cancers; therefore, new strategies are being developed to target such cellular populations. TLR3 activation-based immunotherapy using Polyinosinic:Polycytidylic acid (PIC) has been proposed to be used as a concomitant strategy to first-line treatment. This strategy is based on the induction of apoptosis and an inflammatory response in tumor cells. In combination with retinoids like 9cRA, this treatment can induce CSCs differentiation and apoptosis. A limitation in the use of this combination is the common decreased expression of TLR3 and its main positive regulator p53. observed in many patients suffering of different cancer types such as PCa. Importantly, human exposure to certain toxicants, such as iAs, not only has proven to enrich CSCs population in an in vitro model of human epithelial prostate cells, but additionally, it can also lead to a decreased p53, TLR3 and RA receptor (RARβ), expression/activation and thus hinder this treatment efficacy. Therefore, here we point out the relevance of evaluating the TLR3 and P53 status in PCa patients before starting an immunotherapy based on the use of PIC %2b9cRA to determine whether they will be responsive to treatment. Additionally, the use of strategies to overcome the lower TLR3, RARβ or p53 expression in PCa patients, like the inclusion of drugs that increase p53 expression, is encouraged, to potentiate the use of PIC%2bRA based immunotherapy in these patients. Graphical Abstract: [Figure not available: see fulltext.] © 2022, The Author(s), under exclusive licence to Springer Science%2bBusiness Media, LLC, part of Springer Nature.
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9-cis retinoic acid; Arsenic; Cellular rewiring; Immunotherapy; p53; PIC; Poly (I:C); Prostate cancer; RARβ; TLR3 abiraterone; aldehyde dehydrogenase; alitretinoin; arsenic; arsenite sodium; bicalutamide; cetuximab; chloroquine; dexamethasone; docetaxel; doxorubicin; enzalutamide; erlotinib; gamma interferon; glucocorticoid receptor; goserelin; isotretinoin; leuprorelin; podocalyxin; polycytidylic acid; prostate specific antigen; retinoid; salinomycin; synaptophysin; testosterone; transcription factor Sox2; transcriptome; vorinostat; protein p53; toll like receptor 3; acromegaly; active immunotherapy; acute myeloid leukemia; adaptive immunity; androgen deprivation therapy; antigen presenting cell; apoptosis; autophagosome; breast cancer; cancer chemotherapy; cancer staging; cancer stem cell; cancer susceptibility; carcinogenesis; cell cycle progression; cell differentiation; cell migration; cell plasticity; cell population; cell proliferation; cell survival; clonogenesis; digital rectal examination; DNA methylation; gene silencing; genetic transfection; Gleason score; glioblastoma; hypoxia; immune response; immunotherapy; in vitro study; innate immunity; Lewis carcinoma; male; melanoma; membrane depolarization; mitochondrial respiration; mouse; mouth injury; nuclear reprogramming; obesity; pancreas cancer; peripheral blood mononuclear cell; prevalence; principal component analysis; promyelocytic leukemia; prostate adenocarcinoma; prostate biopsy; prostate cancer; prostate cell; prostatectomy; retrospective study; Review; signal transduction; spliceosome; transcription elongation; tumor cell; tumor growth; tumor microenvironment; ubiquitination; genetics; human; metabolism; pathology; prostate; prostate tumor; stem cell; tumor recurrence; Humans; Male; Neoplasm Recurrence, Local; Prostate; Prostatic Neoplasms; Stem Cells; Toll-Like Receptor 3; Tumor Suppressor Protein p53
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