LncRNA TP53TG1 plays an anti-oncogenic role in cervical cancer by synthetically regulating transcriptome profile in HeLa cells
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ABSTRACT:
PROVIDER: PRJNA851046 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19754142_1.fastq.gz | Fastqsanger.gz | |||
| SRR19754142_2.fastq.gz | Fastqsanger.gz | |||
| SRR19754143_1.fastq.gz | Fastqsanger.gz | |||
| SRR19754143_2.fastq.gz | Fastqsanger.gz | |||
| SRR19754144_1.fastq.gz | Fastqsanger.gz |
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Project description:Long non-coding RNAs (lncRNAs) have been extensively studied as key regulators of cancer development in various cancers. TP53TG1 is a newly identified lncRNA in recent years, and several studies have shown that TP53TG1 may play oncogenic or anti-oncogenic roles in different cancers. Pan-cancer analysis showed that high TP53TG1 expression was significantly associated with better prognosis. Nevertheless, the role of TP53TG1 in the development of cervical cancer is unclear. In our study, we constructed a TP53TG1 overexpression model in HeLa cell line. We found that TP53TG1 overexpression significantly inhibited cell proliferation and induced apoptosis, and TP53TG1 may be a novel anti-oncogenic factor in cervical cancer. Mechanistically, overexpression of TP53TG1 could activate type I interferon signaling pathways and inhibits the expression of genes involved in DNA damage responses. Meanwhile, TP53TG1 could regulate the expression of a large number of RNA binding protein genes thereby potentially affecting the alternative splicing of genes involved in cell proliferation or apoptosis regulation. We also established a ceRNA network to predict the regulatory effect of TP53TG1 on gene expression through miRNA. Our study highlights the essential role of lncRNA TP53TG1 in the development of cervical cancer and suggests the potential regulatory mechanisms.
2022-09-22 | GSE206471 | GEO
Project description:Long non-coding RNAs (lncRNAs) have been extensively studied as important regulators of tumor development in various cancers. Tumor protein 53 target gene 1 (TP53TG1) is a newly identified lncRNA in recent years, and several studies have shown that TP53TG1 may play oncogenic or anti-oncogenic roles in different cancers. Nevertheless, the role of TP53TG1 in the development of cervical cancer is unclear. In our study, pan-cancer analysis showed that high expression of TP53TG1 was significantly associated with a better prognosis. We then constructed a TP53TG1 overexpression model in HeLa cell line to explore its functions and molecular targets. We found that TP53TG1 overexpression significantly inhibited cell proliferation and induced apoptosis, demonstrating that TP53TG1 may be a novel anti-oncogenic factor in cervical cancer. Furthermore, overexpression of TP53TG1 could activate type I interferon signaling pathways and inhibit the expression of genes involved in DNA damage responses. Meanwhile, TP53TG1 could affect alternative splicing of genes involved in cell proliferation or apoptosis by regulating the expression of many RNA-binding protein genes. Competing endogenous RNA (ceRNA) network analysis demonstrated that TP53TG1 could act as the sponge of several miRNAs to regulate the expression level of target genes. In conclusion, our study highlights the essential role of lncRNA TP53TG1 in the development of cervical cancer and suggests the potential regulatory mechanisms.
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Project description:FSCN1 has been reported to be dysregulated in cervical cancers. However, the genome-wide regulated targets of FSCN1 is still unclear in cervical cancers. Here, the gene expression profile of HeLa cells transfected with FSCN1 shRNA (shFSCN1) were compared with cells transfected with empty vector (shCtrl). The results showed that shFSCN1 extensively affects the transcriptional level of 5, 043 genes in HeLa cells. There were more up-regulated genes (3, 870) than down-regulated ones (1, 173) after FSCN1 was knocked down in HeLa cells. GO analysis showed that the up-regulated genes were associated with transcription regulation and DNA binding. The down-regulated genes were enriched in some cancer associated pathway including angiogenesis and cell adhesion. In particular, FSCN1 positilvely regulated ANGPTL4 in HeLa cells. Compared to normal tissue, both FSCN1 and ANGPTL4 showed a higher expression in cervical tumor tissue. Moreover, ANGPTL4 was also positilvely correlated with expression of FSCN1 in cervical tumor tissue of TCGA. In conclusion, our study provide important cues for further study on the regulatory mechanism of FSCN1 in cervical cancer.
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Project description:We aimed to compare the exosomal microRNA profile form HeLa cell line with that from human cervical epithelial cell(Hcer)line.exosomes were isolated from conditioned medium of HeLa cell and HCer cell,3 samples for each group.Exosomal microRNAs were sequenced on Proton Sequencers according to Ion PI Hi-Q Sequencing 200 Kit (Life Technologies).According to the results of miRNA sequencing, we found a total 371 different miRNAs the amount of which reach to 10 fold differece between two groups.
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Project description:Cervical adenocarcinoma (AC), a subtype of uterine cervical cancer (CC), poses a challenge due to its resistance to therapy and poor prognosis compared with squamous cervical carcinoma. Streptococcus agalactiae [group B Streptococcus (GBS)], a Gram-positive coccus, has been associated with cervical intraepithelial neoplasia in CC. However, the underlying mechanism interaction between GBS and CC, particularly AC, remains elusive. Leveraging The Cancer Genome Atlas public data and time-series transcriptomic data, the present study investigated the interaction between GBS and AC, revealing activation of two pivotal pathways: ‘MAPK signaling pathway’ and ‘mTORC1 signaling’. Western blotting, reverse transcription-quantitative PCR and cell viability assays were performed to validate the activation of these pathways and their role in promoting cancer cell proliferation. Subsequently, the present study evaluated the efficacy of two anticancer drugs targeting these pathways (binimetinib and ridaforolimus) in AC cell treatment. Binimetinib demonstrated a cytostatic effect, while ridaforolimus had a modest impact on HeLa cells after 48 h of treatment, as observed in both cell viability and cytotoxicity assays. The combination of binimetinib and ridaforolimus resulted in a significantly greater cytotoxic effect compared to monotherapy, even though the synergy score indicated an additive effect. Furthermore, this drug combination may enhance the effect on HeLa cells exposed to GBS compared to those without exposure. In general, the MAPK and mTORC1 signaling pathways were identified as the main pathways associated with GBS and AC cells. The combination of binimetinib and ridaforolimus could be a potential AC treatment.
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Project description:Persistent infection by high-risk human papillomaviruses (HPVs) is associated with the development of cervical cancer and a subset of anogenital and head and neck squamous cell carcinomas. Abnormal expression of cellular microRNAs (miRNAs) plays an important role in the development of cancer, including HPV-related tumors. MiRNA expression profile was investigated by microrray analysis in the HPV-positive cervical cancer cell lines SiHa (HPV16-positive cell line derived from a cervical squamous cell carcinoma), CaSki (HPV16-positive cell line derived from a metastatic cervical epidermoid carcinoma), and HeLa (HPV18-positive cell line derived from a cervical adenocarcinoma) and compared with primary HFKs and C33a (HPV-negative cervical cell line).
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Project description:It has been well-known that cancer cells acquire approximately three-fold radioresistance under hypoxia than under normoxia due to both radiation chemical and radiation biological mechanisms, causing a negative impact on the outcome of radiation therapy. In the present study, to identify genes responsive to hypoxia in human cervical epithelial adenocarcinoma HeLa cells, global-scale gene expression analysis was carried out using a GeneChip® system.
2020-11-13 | GSE161393 | GEO
Project description:Infection with oncogenic human papillomavirus (HPV) is a major cause for the development of cervical cancer, which is mainly driven by the expression of the HPV E6 and E7 oncoproteins. We uncovered that the concentration levels of the putative tumor suppressor Dickkopf-1 (Dkk1) are restricted in cervical cancer cells by HPV E6 expression due to the E6-mediated proteolytic degradation of p53, which is a transcriptional regulator of Dkk1. Moreover, we found that Dkk1 is critically involved in the pro-apoptotic Cisplatin response of these cells, as Dkk1 repression was associated with an increased resistance towards the chemotherapeutic compound. This could be of high relevance for cervical cancer treatments, which usually involve Cisplatin for standard care. Although Dkk1 is a major antagonist of the canonical Wnt signaling, the differential response towards Cisplatin observed in Dkk1-depleted cells was not associated to an activation of this pathway. To elucidate alternative underlying mechanisms, we performed Affymetrix Gene Expression analyses comparing the transcriptome of Cisplatin-treated parental HeLa to CRISPR/Cas9-generated Dkk1 knockout (KO) HeLa cells. These revealed that Dkk1 depletion is linked to an impairment of the pro-apoptotic JNK/AP-1 pathway in cervical cancer cells, suggesting that Dkk1 drives Cisplatin-mediated apoptosis via activation of this signaling hub.
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2017-09-06 | GSE103475 | GEO
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2022-08-03 | GSE209928 | GEO