Exosomal MicroRNA-223, MicroRNA-146, and MicroRNA-21 Profiles and Biochemical Changes in Laryngeal Cancer

Genç, Sıdıka; Yağcı, Tarık; Vageli, Dimitra P.; Dündar, Rıza; Doukas, Panagiotis G.; Doukas, Sotirios G.; Tolia, Maria; Chatzakis, Nikolaos; Tsatsakis, Aristidis; Taghizadehghalehjoughi, Ali̇

doi:10.1021/acsptsci.3c00038

Cited by 4 publications

(1 citation statement)

References 56 publications

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“…Most abundantly expressed small non-coding RNA better known as miRNA plays an important role in cancer progression by targeting subcellular proteins at post-transcriptional or -translational levels (Calin and Croce 2006 ; Hwang et al 2023 ). One of the most interesting features of a miRNA exhibited a context-dependency via regulating multiple targets even in the same cancer types (Genc et al 2023 ). MiR-29 family consists of three members, encoded by two different genomic loci at chromosome 1 and 7.…”

Section: Introductionmentioning

confidence: 99%

MiR-29 and MiR-140 regulate TRAIL-induced drug tolerance in lung cancer

Kim,

Lee,

Yoo

et al. 2024

Animal Cells and Systems

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has chemotherapeutic potential as a regulator of an extrinsic apoptotic ligand, but its effect as a drug is limited by innate and acquired resistance. Recent findings suggest that an intermediate drug tolerance could mediate acquired resistance, which has made the main obstacle for limited utility of TRAIL as an anti-cancer therapeutics. We propose miRNA-dependent epigenetic modification drives the drug tolerant state in TRAIL-induced drug tolerant (TDT). Transcriptomic analysis revealed miR-29 target gene activation in TDT cells, showing oncogenic signature in lung cancer. Also, the restored TRAIL-sensitivity was associated with miR-29ac and 140-5p expressions, which is known as tumor suppressor by suppressing oncogenic protein RSK2 (p90 ribosomal S6 kinase), further confirmed in patient samples. Moreover, we extended this finding into 119 lung cancer cell lines from public data set, suggesting a significant correlation between TRAIL-sensitivity and RSK2 mRNA expression. Finally, we found that increased RSK2 mRNA is responsible for NF-κB activation, which we previously showed as a key determinant in both innate and acquired TRAIL-resistance. Our findings support further investigation of miR-29ac and - 140-5p inhibition to maintain TRAIL-sensitivity and improve the durability of response to TRAIL in lung cancer.

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Section: Introductionmentioning

confidence: 99%

MiR-29 and MiR-140 regulate TRAIL-induced drug tolerance in lung cancer

Kim,

Lee,

Yoo

et al. 2024

Animal Cells and Systems

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Exploring salivary exosomes as early predictors of oral cancer in susceptible tobacco consumers: noninvasive diagnostic and prognostic applications

Bano,

Vats,

Verma

et al. 2023

J Cancer Res Clin Oncol

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miR‐30a‐3p inhibits the proliferation of laryngeal cancer cells by targeting DNMT3a through regulating DNA methylation of PTEN

Gao,

Ren,

et al. 2023

Oncologie

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Objectives The study aims to examine how miR-30a-3p impacts the growth of laryngeal cancer by exploring its underlying mechanism. Our hypothesis suggests that the regulation of DNMT3a through PTEN by miR-30a-3p plays a significant role in the proliferation of laryngeal cancer. Methods To predict the role of miR-30a-3p in laryngeal cancer and its binding site to DNA methyltransferase 3a (DNMT3a), we utilized data from TCGA, GEO, and starBase. We employed Western blot and qRT-PCR to measure the expression levels of miR-30a-3p, DNMT3a, and PTEN. The interaction between miR-30a-3p and DNMT3a was evaluated using a Luciferase reporter assay. Cell proliferation and invasive abilities were assessed through the CCK-8 kit, EdU staining, and transwell assays. Results Analysis of TCGA data revealed that the expression of miR-30a-3p could impact the survival of patients with head and neck cancer. In Hep-2 cells, we observed down-regulated miR-30a-3p and up-regulated DNMT3a, with a negative correlation between the two. Furthermore, we discovered that miR-30a-3p directly targeted DNMT3a and suppressed its expression in Hep-2 cells, resulting in a decrease in cellular proliferation and invasive capabilities. Additionally, overexpression of miR-30a-3p in Hep-2 cells activated PTEN by reducing DNMT3a expression. Conclusions Our findings indicate that miR-30a-3p, acting as a tumor suppressor gene, plays a regulatory role in the growth and progression of laryngeal cancer through its interaction with DNMT3a and PTEN.

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Exosomal MicroRNA-223, MicroRNA-146, and MicroRNA-21 Profiles and Biochemical Changes in Laryngeal Cancer

Cited by 4 publications

References 56 publications

MiR-29 and MiR-140 regulate TRAIL-induced drug tolerance in lung cancer

MiR-29 and MiR-140 regulate TRAIL-induced drug tolerance in lung cancer

Exploring salivary exosomes as early predictors of oral cancer in susceptible tobacco consumers: noninvasive diagnostic and prognostic applications

miR‐30a‐3p inhibits the proliferation of laryngeal cancer cells by targeting DNMT3a through regulating DNA methylation of PTEN

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