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GLIDR-mediated Regulation of Tumor Malignancy and Cisplatin Resistance in Non-Small Cell Lung Cancer via the miR-342-5p/PPARGC1A Axis

ABSTRACT: GLIDR-mediated Regulation of Tumor Malignancy and Cisplatin Resistance in Non-Small Cell Lung Cancer via the miR-342-5p/PPARGC1A Axis

PROVIDER: PRJNA1018525 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26103089_1.fastq.gz	Fastqsanger.gz
	SRR26103089_2.fastq.gz	Fastqsanger.gz
	SRR26103090_1.fastq.gz	Fastqsanger.gz
	SRR26103090_2.fastq.gz	Fastqsanger.gz
	SRR26103091_1.fastq.gz	Fastqsanger.gz

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GLIDR-mediated Regulation of Tumor Malignancy and Cisplatin Resistance in Non-Small Cell Lung Cancer via the miR-342-5p/PPARGC1A Axis

Project description:LncRNAs play a crucial role in regulating the progression of NSCLC, making them potential targets for cancer diagnosis and treatment. Therefore, identifying new lncRNAs as therapeutic target and comprehending their underlying regulatory mechanisms are crucial for treating NSCLC. In this study, we found that glioblastoma down-regulated RNA (GLIDR) was increased in non-response NSCLC patients with the primary treatment, and GLIDR was also highly expressed in NSCLC patients. We used bioinformatic analysis and luciferase assays to identify that microRNA-342-5p (miR-342-5p) directly targets GLIDR. MiR-342-5p overexpression inhibits NSCLC cell proliferation, migration, and invasion, whereas miR-342-5p inhibition promotes NSCLC malignancy, which can be rescued by suppressing GLIDR. Peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PPARGC1A) was identified as a downstream target of miR-342-5p. PPARGC1A inhibition significantly suppresses NSCLC malignancy, whereas overexpression promotes it. The results also revealed that GLIDR overexpression reduced PPARGC1A inhibition by miR-342-5p, and increased PPARGC1A expression reversed the inhibition of NSCLC malignancies caused by decreased GLIDR. To the best of our knowledge, we are the first to discover that GLIDR promotes NSCLC progression by sponging miR-342-5p to regulate PPARGC1A expression, presenting that GLIDR act as a potential therapeutic target in NSCLC.

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Gene expression analysis to find molecular mechanisms underlying the role of miR-342-5p in HER2 breast cancer

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Circ_0008146 exacerbates ferroptosis via regulating miR-342-5p/ACSL4 axis after cerebral ischemia-reperfusion in mice

Project description:Background: Characterized by high incidence, mutilation, and death rate, acute ischemic stroke (AIS) has threatened people’s health seriously. Therefore, there is an urge need for early diagnosis and effective treatment of AIS. The purpose of this study was to clarify the regulatory role and potential molecular mechanism of miR-342-5p and circRNA_0008146 in AIS. Materials and Methods: Small RNA sequencing analysis was performed to screen differentially expressed miRNAs between the AIS and control group. Middle cerebral artery occlusion/reperfusion (MCAO/R) models were constructed in C57BL/6J mice. The circRNA_0008146 and miRNA expression levels were detected by quantitative real-time PCR. Assay kits were used to determine Fe2+ levels and assess a battery of oxidative stress indicators, including ROS, MDA, LPO, SOD, and GSH/GSSG. The content of ACSL4 was measured by Western blot. The neurobehavioral manifestation was evaluated using the modified Neurological Severity (mNSS) Score, rotarod test, and corner test. TTC staining was employed to detect cerebral infarction volume. Nissl staining was adapted to detect histological change and neuronal damage. Results: RNA sequencing analysis revealed miR-342-5p was significantly downregulated in the plasma of AIS patients. MiR-342-5p inhibited oxidative stress and RSL3-induced ferroptosis after cerebral ischemic-reperfusion injury in vivo by targeting ferroptosis-related gene ACSL4. CircRNA_0008146 acted as a sponge of miR-342-5p, and overexpression of circRNA_0008146 increased brain damage in stroke mice. CircRNA_0008146 contributed to ferroptosis in cerebral infraction via sponging miR-342-5p to regulate ACSL4. Conclusion: CircRNA_0008146/miR-342-5p/ACSL4 axis regulate ferroptosis after cerebral ischemia-reperfusion, which may be a potential therapeutic target for ischemic stroke.

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Project description:Purpose:In recent years, increasing evidence has confirmed that exosomal circular RNAs (circRNAs) play a crucial role in the prognostic prediction and diagnosis of liver cancer （LC）. In this study, we first compared the expression patterns of exosomal circRNAs during transarterial chemoembolization (TACE). Methods:CircRNA-seq identified 390 differentially expressed circRNAs between the prior TACE and TACE1 groups and 489 differentially expressed circRNAs between the prior TACE and TACE2 groups. GO analysis of the differentially expressed circRNAs showed that they were associated with fatty acid metabolism, receptor binding and membrane protein complexes. KEGG pathway analysis predicted that protein digestion and absorption pathways were activated after TACE. And we screened out a novel gene , hsa_circRNA_G004213 (circ_G004213) was significantly upregulated after TACE (fold change >10, P<0.01). Further analysis found circ_G004213 significantly increased the cisplatin sensitivity of HepG2 cells and positively correlated with the prognosis of tumor-bearing mice. Based on the potential downstream miRNAs and mRNAs, the circRNA‐miRNA-mRNA network was constructed. Results: We demonstrated that circ_G004213 regulates cisplatin resistance via the miR-513b-5p/PRPF39 axis. Finally, our study confirmed that circ_G004213 was positively correlated with the prognosis of LC patients after TACE. Therefore, circ_G004213 may be used as an indicator for predicting the efficacy of TACE. Conclusions: Hsa_circRNA_G004213 Promotes Cisplatin Sensitivity by Regulating miR-513b-5p/PRPF39 in Liver Cancer.

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