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Tumor suppressive long non-coding RNA AFDN-DT inhibits gastric cancer invasion via transcriptional regulation

ABSTRACT: Tumor suppressive long non-coding RNA AFDN-DT inhibits gastric cancer invasion via transcriptional regulation

PROVIDER: PRJNA579322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10341052_1.fastq.gz	Fastqsanger.gz
	SRR10341052_2.fastq.gz	Fastqsanger.gz
	SRR10341053_1.fastq.gz	Fastqsanger.gz
	SRR10341053_2.fastq.gz	Fastqsanger.gz
	SRR10341054_1.fastq.gz	Fastqsanger.gz

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Tumor suppressive long non-coding RNA AFDN-DT inhibits gastric cancer invasion via transcriptional regulation

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Tumour suppressive long non-coding RNA AFDN-DT inhibits gastric cancer invasion via transcriptional regulation.

Project description:Emerging evidence has revealed that dysregulation of lncRNA is associated with the initiation and progression of cancer. However, the function of these lncRNAs in cancer remains largely unexplored. Here, we reported that AFDN-DT, an lncRNA that is repressed in gastric cancers (GC), functions as a tumour suppressor by inhibiting cell growth and metastasis through transcriptional repression of genes involved in metastasis. Using in vitro and in vivo models, we demonstrated that overexpression of AFDN-DT inhibited the proliferation and metastasis of GC. We found that AFDN-DT was located at the nucleus and interacted with the chromatin in gastric cells. Further, ChIRP-seq experiments and RNA-seq analysis revealed that AFDN-DT directly bound to the promoter regions and regulated the expression of genes essential for malignant transformation. Moreover, we demonstrated that DNA hypermethylation could repress AFDN-DT expression and treatment with DNA methylation inhibitors restored its expression. Collectively, the results of our study demonstrated the tumour suppressive role of AFDN-DT in GC and elucidated the transcription regulatory role of tumour suppressive lncRNAs, which can serve as potential prognostic markers for GC.

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Delftia sp. DT strain:DT | isolate:intestine

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Tumor‑suppressive miR‑299‑3p inhibits gastric cancer cell invasion by targeting heparanase.

Project description:Gastric cancer (GC) remains a leading cause of cancer‑associated mortality globally. Emerging evidence suggests that microRNAs (miRs) function as oncogenes or tumor suppressors, contributing to various aspects of cancer progression, including invasion and metastasis. In the present study, the specific role of miR‑299‑3p in the invasion of GC cells was investigated. The expression level of miR‑299‑3p was measured using reverse transcription‑quantitative PCR and in situ hybridization in human GC tissues. Effects of miR‑299‑3p on GC cell invasion were determined by Transwell assay. Bioinformatics and luciferase reporter assays were performed to identify and verify the downstream effectors of miR‑299‑3p. miR‑299‑3p expression analysis in clinical GC samples revealed a significant downregulation of miR‑299‑3p compared with non‑tumor tissues. Inhibition of miR‑299‑3p promoted the invasive abilities of GC cells, whereas its overexpression significantly suppressed cell invasion. Bioinformatics and luciferase reporter assays identified heparanase (HPSE) as a direct target of miR‑299‑3p, the ectopic expression of which reversed the impairment in cell invasion induced by miR‑299‑3p upregulation. Furthermore, HPSE expression was negatively associated with miR‑299‑3p levels in human GC tissues. Overall, the present study indicated that miR‑299‑3p functions as a tumor suppressor by directly targeting HPSE, highlighting its potential as a target for the treatment of GC.

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In vitro organoid-based assays reveal SMAD4 tumor-suppressive mechanisms for serrated colorectal cancer invasion [RNA-seq]

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