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Arsenic trioxide regulates DYNAP through hsa-mir-573 and inhibits the proliferation of laryngeal cancer

ABSTRACT: Arsenic trioxide regulates DYNAP through hsa-mir-573 and inhibits the proliferation of laryngeal cancer

PROVIDER: PRJNA1268913 | ENA |

REPOSITORIES: ENA

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Arsenic trioxide regulates DYNAP through hsa-mir-573 and inhibits the proliferation of laryngeal cancer

Project description:BACKGROUND: Laryngeal squamous cell carcinoma (LSCC) is a malignant tumor with limited treatment options and poor prognosis in advanced stages. Arsenic trioxide (ATO), a drug well-known for treating acute promyelocytic leukemia, has shown potential antitumor effects in several solid tumors. This study aimed to investigate the role of ATO on LSCC proliferation and its underlying molecular mechanisms. METHODS: LSCC cell lines (TU212, TU686, and AMC-HN-8) were treated with varying concentrations of ATO, and cell proliferation was evaluated using CCK-8, colony formation, and EdU assays. miRNA-sequencing identified differentially expressed miRNAs after ATO treatment, and bioinformatics tools predicted hsa-miR-573 target genes. The interaction between hsa-miR-573 and dynactin-associated protein (DYNAP) was validated by dual-luciferase reporter assays. Additionally, a xenograft tumor model was established to examine the in vivo effects of ATO on tumor growth. RESULTS: ATO significantly inhibited LSCC cell proliferation in a dose- and time-dependent manner. miRNA-sequencing identified hsa-miR-573 as significantly upregulated following ATO treatment, and functional studies demonstrated that hsa-miR-573 suppresses LSCC cell proliferation by directly targeting DYNAP. Overexpression of DYNAP promoted LSCC cell proliferation, while DYNAP knockdown reversed this effect. In vivo, ATO treatment suppressed tumor growth in nude mice without significant nephrotoxicity or cardiotoxicity. Mechanistically, ATO reduced the expression of DYNAP and inhibited the PI3K/AKT signaling pathway. CONCLUSION: ATO inhibited LSCC progression by upregulating hsa-miR-573, which directly targets DYNAP to suppress cell proliferation and disrupt the PI3K/AKT signaling pathway. These findings supported the potential of ATO as a therapeutic agent for LSCC.

2025-08-06 | GSE298303 | GEO

Aberrantly expressed genes in HaCaT keratinocytes chronically exposed to arsenic trioxide

2012-04-12 | GSE37192 | GEO

Aberrantly expressed genes in HaCaT keratinocytes chronically exposed to arsenic trioxide

Project description:The purpose of this study is to search for aberrant genes in HaCaT keratinocytes after chronic exposure to arsenic trioxide. The objective of the investigation was to discover the mechanism of arsenic carcinogenicity in human epidermal keratinocytes. We hypothesize that a combined strategy of DNA microarray, qRT-PCR and gene function annotation will identify aberrantly expressed genes in HaCaT keratinocyte cell line after chronic treatment with arsenic trioxide. HaCaT cells were chronically exposed to 0.5M-BM-5g/mL arsenic trioxide (As2O3) up to 22 passages and RNA was extracted. Microarray data analysis identified 14 up-regulated genes and 21 down-regulated genes in response to arsenic trioxide Two experimental groups: 1. The treatment group was sub-cultured up to passage 22 to establish a chronic exposure state. 2. The passage control group was also sub-cultured up to 22 passages but with no exposure to arsenic trioxide. 4 technical replicates with 3 replicates making a total of 8X3 =24 samples HaCat Cell untreated (passage control): 1. H1_H001, H1_H002, H1_H003 2. H2_ H004, H2_H005, H2_H006 3. H3_ H007, H3_H008, H3_H009 4. H4_ H010, H4_H011, H4_H012 HaCat Cell treated with 0.5M-BM-5g/ml of arsenic trioxide: 5. A1_H013, A1_H014, A1_H015 6. A2_H016, A2_H017, A2_H018 7. A3_H019, A3_H020, A3_H021 8. A4_H022, A4_H023, A4_H024 Cell Type: Human Skin Keratinocyte: 1.5 M-CM-^W105 HaCaT cells were cultured in 7.5 ml of complete DMEM containing 10% Fetal Bovine Serum (FBS) and 1% penicillin, streptomycin in T-25 culture plate. Cells were incubated in a humidified atmosphere with 5% CO2 at 37 M-BM-:C. The treatment groups were exposed to 0.5M-BM-5g/mL As2O3 (equivalent to LC 0.5), and passaged at 90% confluent. Total RNA was extracted from 4 technical replicates of unexposed HaCaT cells and HaCaT cells chronically exposed to arsenic trioxide up to passage 22 using RNA STAT-60 (TEL-TEST, INC, Friendswood, TX, USA).

2012-04-11 | E-GEOD-37192 | biostudies-arrayexpress

Transcriptome analysis of mutant p53 rescued by arsenic trioxide (ATO)

Project description:The goals of this study are to compare transcriptome of mutant p53 rescued by arsenic trioxide

2022-12-12 | GSE141892 | GEO

Identification of differentially expressed genes by rapid induction of PML/RARa degradation using arsenic trioxide in NB4 cells

Project description:Acute promyelocytic leukemia (APL) is characterized by the specific chromosome translocation t(15;17) that generates the promyelocytic leukemia/retinoic acid receptor-α (PML/RARα) fusion gene. Arsenic trioxide has been intensively reported to directly and rapidly degrade the PML/RARα fusion protein. Here, we treated NB4 cells (a widely used APL cell line) with arsenic trioxide and performed RNA-seq analysis to identify differentially expressed genes upon arsenic trioxide treatment.

2025-02-14 | GSE126623 | GEO

Transcriptome analysis of mutant p53 (p53-V272M, p53-R282W) rescued by arsenic trioxide (ATO)

Project description:The goals of this study are to compare transcriptome of mutant p53 rescued by arsenic trioxide

2023-06-03 | GSE151696 | GEO

The genomic landscape of sensitivity to Arsenic Trioxide characterized by Genome-wide CRISPR-Cas9 screening

Project description:The key modifiers of sensitivity to Arsenic Trioxide (ATO) remained unclear, and we presented a genome-wide scale loss-of-function screening to identify the modulators of cell response to ATO.

2023-04-24 | GSE218982 | GEO

Comparison of gene expression profile of naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

Project description:The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide (ATO). The gene expression profile of naive (NB4) (Acute promyelocytic leukemia (APL) cell line and one of its in house generated ATO resistant sub clone (NB4-VM-AsR1) was done using whole genome microarray and compared to generate the differential expression profile which will give insight into the mechanisms of ATO resistance in APL. Agilent one-color experiment,Organism: Human ,Agilent Whole Genome Human 4x44k (AMADID: 014850) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

2013-08-02 | E-GEOD-42031 | biostudies-arrayexpress

Arsenic Trioxide, Fluorouracil, and Leucovorin in Treating Patients With Stage IV Colorectal Cancer That Has Relapsed or Not Responded to Treatment

Project description:RATIONALE: Drugs used in chemotherapy, such as fluorouracil and leucovorin, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. Arsenic trioxide may help fluorouracil and leucovorin work better by making tumor cells more sensitive to the drugs. Giving arsenic trioxide together with fluorouracil and leucovorin may kill more tumor cells. PURPOSE: This phase I trial is studying the side effects and best dose of arsenic trioxide and fluorouracil when given together with leucovorin in treating patients with stage IV colorectal cancer that has relapsed or not responded to treatment.

| 2038167 | ecrin-mdr-crc

Clinical trial of intravenous arsenic trioxide in the treatment of advanced refractory colorectal cancer carrying structural mutant p53 gene

Project description:Interventions: Experimental group:intravenous arsenic trioxide Primary outcome(s): Objective response rate Study Design: Single arm

| 2692740 | ecrin-mdr-crc

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