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Circular RNA YPEL2 promotes cell proliferation, migration and invasion as a biomaker in cervical cancer

ABSTRACT: Circular RNA YPEL2 promotes cell proliferation, migration and invasion as a biomaker in cervical cancer

PROVIDER: PRJNA723838 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14301221_1.fastq.gz	Fastqsanger.gz
	SRR14301221_2.fastq.gz	Fastqsanger.gz
	SRR14301222_1.fastq.gz	Fastqsanger.gz
	SRR14301222_2.fastq.gz	Fastqsanger.gz
	SRR14301223_1.fastq.gz	Fastqsanger.gz

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Circular RNA YPEL2 promotes cell proliferation, migration and invasion as a biomaker in cervical cancer

Project description:Circular RNA (circRNA) is newly type of noncoding RNA that are formed by back-splicing of exon and play the important functions in tumorigenesis. However, the research of circRNA is deficient in cervical cancer (CC). We performed high-throughput sequencing on cervical cancer tissues and normal cervical control samples. We discovered the up-regulated circYPEL2 (has_circ_0005400) in cervical cancer and used this as a potential research object through bioinformatics analysis. Finally, through RNA sequencing and bioinformatics technology, we analyzed the downstream targeted genes that may be affected by circYPEL2.

2022-01-31 | GSE173112 | GEO

TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy [MeDIP-Seq]

Project description:Methylation modifications play pertinent roles in regulating gene expression and various biological processes. The silencing of the demethylated modifier TET1 can affect the expressions of key oncogenes or tumor suppressor genes, thus contributing to tumor formation. Nonetheless, how TET1 affects the progression of cervical cancer is yet to be elucidated. In this study, we found that the expression of TET1 was significantly downregulated in cervical cancer tissues. Functionally, TET1 knockdown in cervical cancer cells can promote cell proliferation, migration, invasion, cervical xenograft tumor formation and EMT. On the contrary, its overexpression can reverse the aforementioned processes. Moreover, the autophagy level of cervical cancer cells can be enhanced after TET1 knockdown. Mechanistically, methylated DNA immunoprecipitation (MeDIP)-sequencing and MeDIP quantitative real-time PCR revealed that TET1 mediates the methylation of autophagy promoter regions. These findings suggest that TET1 affects the malignant biological behavior of cervical cancer cells by altering the methylation levels of autophagy genes NKRF and HIST1H2AK, but the specific mechanism needs to be investigated further.

2024-03-13 | GSE236315 | GEO

TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy [RNA-seq]

2024-03-13 | GSE236396 | GEO

MicroRNA‑130a‑3p inhibition suppresses cervical cancer cell progression

Project description:MicroRNAs (miRNAs or miRs) play essential roles in the initiation and progression of human tumors, including cervical cancer. However, the mechanisms underlying their actions in cervical cancer remain unclear. The present study aimed to evaluate the functional role of miR‑130a‑3p in cervical cancer. Cervical cancer cells were transfected with a miRNA inhibitor (anti‑miR‑130a‑3p) and a negative control. Adhesion‑independent cell proliferation, migration and invasion were evaluated. The findings presented herein demonstrated that miR‑130a‑3p was overexpressed in HeLa, SiHa, CaSki, C‑4I and HCB‑514 cervical cancer cells. The inhibition of miR‑130a‑3p significantly reduced the proliferation, migration and invasion of cervical cancer cells. The canonical delta‑like Notch1 ligand (DLL1) was identified as a possible direct target of miR‑103a‑3p. The DLL1 gene was further found to be significantly downregulated in cervical cancer tissues. On the whole, the present study demonstrates that miR‑130a‑3p contributes to the proliferation, migration and invasion of cervical cancer cells. Therefore, miR‑130a‑3p may be used as a biomarker to determine cervical cancer progression.

2023-03-10 | GSE224301 | GEO

Targeting the Epigenome Reduces Keloid Fibroblast Cell Proliferation, Migration and Invasion

Project description:Targeting the Epigenome Reduces Keloid Fibroblast Cell Proliferation, Migration and Invasion

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TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy

Project description:TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy

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circ_0000045 promotes proliferation, migration, and invasion of head and neck squamous cell carcinomas via binding with HSP70 and MAPK signaling activation

Project description:Objective: Head and neck squamous cell carcinoma (HNSCC) is one severe malignancy driven by complex cellular and signaling mechanisms. However, the roles of circular RNAs (circRNAs) in HNSCC’s development remains poorly understood. Therefore, this study investigated the functions of differentially expressed circRNAs in regulating HNSCC cell functions. Methods: Differentially expressed circRNAs were characterized through RNA sequencing in HNSCC tissues. CircRNA’s identity was then confirmed using RT-PCR and Sanger’s sequencing. Next, expression levels of circRNA and mRNA were detected by qRT-PCR, after which protein abundances were measured by Western blotting. Subsequently, the proliferation, migration, and invasion of HNSCC cells was assessed by MTS, wound healing, and Transwell system, respectively, followed by identification of circRNA-binding proteins in HNSCC cells by circRNA pull-down, coupled with mass spectrometry. Results: Great alterations in circRNA profiles were detected in HNSCC tissues, including the elevated expression of circ_0000045. As observed, silencing of circ_0000045 effectively repressed the proliferation, migration, and invasion of HNSCC cell lines (FaDu and SCC-9). Contrarily, circ_0000045’s overexpression promoted the proliferation, migration, and invasion in FaDu and SCC-9 cells. Results also showed that circ_0000045 was associated with multiple RNA-binding proteins in HNSCC cells, such as HSP70. Moreover, circ_0000045 knockdown enhanced HSP70 expression and promoted JNK2 and P38’s expression in HNSCC cells, which were oppositely regulated by circ_0000045’s overexpression. Conclusion: The high expression of circ_0000045; therefore, promoted cell proliferation, migration, and invasion during HNSCC’s development through association with HSP70 protein to activate mitogen-activated protein kinase signaling.

2022-05-11 | GSE197138 | GEO

Silencing of STEAP3 suppresses cervical cancer cell proliferation and migration via JAK/STAT3 signaling pathway

Project description:To investigate the mechanisms of STEAP3 in cervical cancer cell proliferation and migration, we established HeLa cell lines in which STEAP3 gene has been knocked down by shRNA. We then performed gene expression profiling analysis and enrichment analysis using data obtained from RNA-seq of NC and KD cells.

2024-12-31 | GSE284355 | GEO

MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53

Project description:MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53

| PRJNA1027746 | ENA

MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53

Project description:Aberrantexpression of long non-coding RNAs (lncRNAs) has been reported to play a crucial role in the biological function of trophoblasts and contribute to preeclampsia (PE). Our previous study demonstrated that MIR193BHG is increased in preeclamptic placental tissues. In this study, we further explored the effects of MIR193BHG on the function of trophoblast cells and attempted to elucidate its underlying molecular mechanisms. Results showed that MIR193BHG was predominantly localized in the nucleus of HTR-8/SVneo cells. Overexpression of MIR193BHG significantly inhibited proliferation, migration and invasion of HTR-8/SVneo cells, while increasing apoptosis. Knockdown of MIR193BHG produced opposite effects.Furthermore, overexpression of MIR193BHG led to significant increases in both mRNA and protein levels of p53 compared with the control group. More importantly, knockdown of p53 rescued the negative effects induced by overexpressed MIR193BHG on cell proliferation, migration, and invasion while partially counteracting its apoptotic effects on HTR-8/SVneo cells. In conclusion, our findings suggest that MIR193BHG played a critical role in the progression of PE by regulating the expression of p53 and may serve as a novel therapeutic target for PE.

2023-10-16 | GSE245279 | GEO

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