CircSLCO3A1 depletion ameliorates lipopolysaccharide-induced inflammation and apoptosis of human pulmonary alveolar epithelial cells through the miR-424-5p/HMGB3 pathway

Li, Yan; Zhang, Chunmei; Zhao, Zhongyan

doi:10.1007/s13273-023-00341-6

Cited by 3 publications

(2 citation statements)

References 35 publications

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“…The miR-424-5p miRNA has been strongly associated with various diseases, including hepatocellular carcinoma, ovarian cancer, and NSCLC [ 13 ]. Moreover, the inflammatory factor lncRNA circSLCO3A1 has been found to induce inflammation and apoptosis in human alveolar epithelial cells, which is achieved by competitively sponging with miR-424-5p, thereby activating the HMGB3 axis [ 14 ]. ANLN encodes an actin-binding protein, which is mainly located in the cytoskeleton and nucleus, and plays a role in cell proliferation and migration as well as cytoplasmic division [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

lncRNA CERS6-AS1 upregulates the expression of ANLN by sponging miR-424-5p to promote the progression and drug resistance of lung adenocarcinoma

Ting,

Wu,

Yang

et al. 2024

Non-coding RNA Research

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Section: Introductionmentioning

confidence: 99%

lncRNA CERS6-AS1 upregulates the expression of ANLN by sponging miR-424-5p to promote the progression and drug resistance of lung adenocarcinoma

Ting,

Wu,

Yang

et al. 2024

Non-coding RNA Research

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“…This effect is achieved by competitively binding to miR-424-5p, thereby activating the HMGB3 axis. [14] In this study, our objective was to investigate the function and underlying molecular mechanism of CERS6-AS1 in the progression of LUAD (lung adenocarcinoma). Our findings demonstrated that CERS6-AS1 exhibited significant overexpression in both LUAD tissues and cells.…”

Section: Introductionmentioning

confidence: 99%

lncRNA CERS6-AS1 promotes cell proliferation, migration, invasion, and epithelial-mesenchymal transformation of lung adenocarcinoma by sponging miR-424-5p upregulates ANLN expression

Zhuo,

Wu,

Yang

et al. 2023

Preprint

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Background Long noncoding RNA (lncRNA) plays a crucial role in tumor genesis and progression, exerting strong regulation over cancer cell growth. Among these lncRNAs, one of particular concern is lncRNA CERS6 antisense RNA 1 (CERS6-AS1). Functioning as an oncogene, it exhibits significant upregulation and promotes tumor progression in various types of tumors. However, the exact functional significance and underlying molecular mechanism by which CERS6-AS1 operates in the context of lung adenocarcinoma (LUAD) remain unclear. Methods Expression levels of CERS6-AS1 in both LUAD and normal tissues were examined using RNA data obtained from the Cancer Genome Atlas (TCGA). To validate these findings, the expression of CERS6-AS1 was further assessed in clinical samples and lung cancer cell lines using real-time quantitative polymerase chain reaction (RT-qPCR). Different databases such as TargetScan, ENCORI, and StarBase were utilized to predict potential micro-RNAs (miRNAs) that could bind to CERS6-AS1. Experimental validation of the functional implications of both CERS6-AS1 and miR-424-5p in cell proliferation, migration, and invasion capacity was carried out using cell counting kit-8, wound healing, and Transwell assays. The interaction between CERS6-AS1 and miR-424-5p was investigated through a luciferase assay. Furthermore, multiple databases were used to identify potential downstream genes associated with the regulatory axis of CERS6-AS1/miR-424-5p. A bioinformatics analysis was performed to evaluate the impact of increased expression of the downstream gene ANLN on various factors, including immune cell infiltration, tumor mutation burden, response to chemotherapy, and immunotherapy. Results CERS6-AS1 was observed to be upregulated in both LUAD tissue samples and lung cancer cell lines. To investigate the functional relevance of CERS6-AS1, knockdown experiments were conducted in A549 and H1299 cell lines. The knockdown of CERS6-AS1 significantly inhibited cell proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) in these cell lines. Notably, there was a prominent upregulation of miR-424-5p expression in cells where CERS6-AS1 was knocked down. Co-transfection of si-CERS6-AS1-2 and miR-424-5p inhibitors into lung cancer cells restored the cytological behavior inhibited by CERS6-AS1 knockdown. These findings provide evidence for a targeted relationship between CERS6-AS1 and miR-424-5p. Anillin (ANLN) has been identified as a potential target gene for miR-424-5p, which serves as a prognostic and immunobiomarker associated with immune cell infiltration and tumor mutational burden in LUAD. Additionally, ANLN impacts the efficacy of chemotherapy and immunotherapy in LUAD patients. Conclusion This study unveils a novel regulatory mechanism in which CERS6-AS1 potentially influences ANLN expression by acting as a competitive sponge for miR-424-5p. This regulatory axis is implicated in the progression of lung adenocarcinoma, offering valuable insights for the diagnosis and treatment of this disease.

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Structure and Functions of HMGB3 Protein

Chikhirzhina,

Tsimokha,

Tomilin

et al. 2024

IJMS

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HMGB3 protein belongs to the group of HMGB proteins from the superfamily of nuclear proteins with high electrophoretic mobility. HMGB proteins play an active part in almost all cellular processes associated with DNA—repair, replication, recombination, and transcription—and, additionally, can act as cytokines during infectious processes, inflammatory responses, and injuries. Although the structure and functions of HMGB1 and HMGB2 proteins have been intensively studied for decades, very little attention has been paid to HMGB3 until recently. In this review, we summarize the currently available data on the molecular structure, post-translational modifications, and biological functions of HMGB3, as well as the possible role of the ubiquitin–proteasome system-dependent HMGB3 degradation in tumor development.

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CircSLCO3A1 depletion ameliorates lipopolysaccharide-induced inflammation and apoptosis of human pulmonary alveolar epithelial cells through the miR-424-5p/HMGB3 pathway

Cited by 3 publications

References 35 publications

lncRNA CERS6-AS1 upregulates the expression of ANLN by sponging miR-424-5p to promote the progression and drug resistance of lung adenocarcinoma

lncRNA CERS6-AS1 upregulates the expression of ANLN by sponging miR-424-5p to promote the progression and drug resistance of lung adenocarcinoma

lncRNA CERS6-AS1 promotes cell proliferation, migration, invasion, and epithelial-mesenchymal transformation of lung adenocarcinoma by sponging miR-424-5p upregulates ANLN expression

Structure and Functions of HMGB3 Protein

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