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ABSTRACT
Introduction
Non-coding RNAs (ncRNAs), which are incapable of encoding proteins, are involved in the progression of numerous tumors by altering transcriptional and post-transcriptional processing. Recent studies have revealed prominent features of ncRNAs in pyroptosis, a type of non-apoptotic programmed cellular destruction linked to an inflammatory reaction. Drug resistance has arisen gradually as a result of anti-apoptotic proteins, therefore strategies based on pyroptotic cell death have attracted increasing attention. We have observed that ncRNAs may exert significant influence on cancer therapy, chemotherapy, radio- therapy, targeted therapy and immunotherapy, by regulating pyroptosis.
Areas covered
Literatures were searched (December 2023) for studies on cancer therapy for ncRNAs-mediated pyroptotic cell death.
Expert opinion
The most universal mechanical strategy for ncRNAs to regulate target genes is competitive endogenous RNAs (ceRNA). Besides, certain ncRNAs could directly interact with proteins and modulate downstream genes to induce pyroptosis, resulting in tumor growth or inhibition. In this review, we aim to display that ncRNAs, predominantly long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and circular RNAs (circRNAs), could function as potential biomarkers for diagnosis and prognosis and produce new insights into anti-cancer strategies modulated by pyroptosis for clinical applications.
Article highlights
Non-coding RNAs are involved in tumor progression at the transcriptional and post transcriptional levels.
NcRNAs, including lncRNAs, miRNAs and circRNAs, are of significant importance in regulating pyroptosis.
NcRNAs can potentially play a crucial role in enhancing the effectiveness of cancer treatments, including chemotherapy, radiotherapy, targeted therapy, and immunotherapy, through the modulation of pyroptosis.
The regulatory axis involving lncRNAs, miRNAs, and mRNAs has an important function in the fundamental mechanisms underlying cancer development and progression.
Research on gasdermin C, D and E are more abundant compared to the limited studies concerning other proteins in the gasdermin family.
Abbreviations
| AIM2 | = | absent in melanoma 2 |
| ASC | = | apoptosis-associated speck-like protein |
| ceRNA | = | competitive endogenous RNA |
| circRNAs | = | circular RNAs |
| CRC | = | colorectal cancer |
| CSCs | = | cancer stem cells |
| CS-NSCLC | = | cisplatin-sensitive non-small cell lung cancer |
| CSR-NSCLC | = | cisplatin-resistant non-small cell lung cancer |
| DCs | = | dendritic cells |
| DDP | = | cisplatin |
| DFS | = | disease-free survival |
| DHA | = | dihydroartemisinin |
| DM | = | diabetes mellitus |
| EGFR | = | epidermal growth factor receptor |
| ER | = | estrogen receptor |
| ESCC | = | esophageal squamous cell carcinoma |
| ET | = | endocrine therapy |
| GAS5 | = | growth arrest-specific transcript 5 |
| GC | = | gastric cancer |
| GSDM | = | gasdermin |
| HER2 | = | human epidermal receptor 2 |
| HOTTIP | = | HOXA transcript at the distal tip |
| ICA | = | Icariin |
| IL-1β | = | interleukin-1β |
| IL-18 | = | interleukin-18 |
| lncRNAs | = | long non-coding RNAs |
| LUAD | = | lung adenocarcinoma |
| MEG3 | = | Maternally expressed gene 3 |
| miRNAs | = | microRNAs |
| NACT | = | neo-adjuvant chemotherapy |
| NEAT1 | = | nuclear paraspeckle assembly transcript 1 |
| ncRNAs | = | noncoding RNAs |
| NLRP1 | = | nod-like receptor protein 1 |
| NLRP3 | = | nod-like receptor protein 3 |
| NLRC4 | = | nucleotide-binding oligomerization domain-like receptor protein C4 |
| NSCLC | = | non-small cell lung cancer |
| OC | = | ovarian cancer |
| ORFs | = | open reading frames |
| OS | = | overall survival |
| OSCC | = | oral squamous cell carcinoma |
| PCD | = | programmed cell death |
| PR | = | progesterone receptor |
| PRGs | = | pyroptosis-related genes |
| SIRT1 | = | Sirtuin1 |
| SNHG7 | = | Small nucleolar RNA host gene 7 |
| TGFBI | = | Transforming Growth Factor Beta Induced |
| TME | = | tumor microenvironment |
| TNBC | = | triple-negative breast cancer |
| TKI | = | tyrosine kinase inhibitors |
Declarations of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Acknowledgments
The authors would like to express their appreciation to the Department of Medical Laboratory, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, and the School of Laboratory Medicine, Hubei University of Chinese Medicine, Wuhan, China, for their technology and education.