Long noncoding RNA LINC00857 promotes pancreatic cancer proliferation and metastasis by regulating the miR-130b/RHOA axis

Chen, Peng; Zeng, Zhirui; Wang, Jie; Cao, Wenpeng; Song, Chunzhuo; Lei, Shan; Li, Yichuan; Ren, Zhangxia

doi:10.1038/s41420-022-01008-2

Cited by 14 publications

(8 citation statements)

References 33 publications

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“…4A ). It is worth noting that, among them, linc00857 has been shown to be an oncogenic lncRNA in various cancers [ 16 , 17 ], while GPX4 is one of the essential enzymes involved in ferroptosis. We therefore focused on these two FOXP3 downstream members.…”

Section: Resultsmentioning

confidence: 99%

FOXP3 promote the progression of glioblastoma via inhibiting ferroptosis mediated by linc00857/miR-1290/GPX4 axis

Cao,

He,

Lan

et al. 2024

Cell Death Dis

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The oncogenic properties of members belonging to the forkhead box (FOX) family have been extensively documented in different types of cancers. In this study, our objective was to investigate the impact of FOXP3 on glioblastoma multiforme (GBM) cells. By conducting a screen using a small hairpin RNA (shRNA) library, we discovered a significant association between FOXP3 and ferroptosis in GBM cells. Furthermore, we observed elevated levels of FOXP3 in both GBM tissues and cell lines, which correlated with a poorer prognosis. FOXP3 was found to promote the proliferation of GBM cells by inhibiting cell ferroptosis in vitro and in vivo. Mechanistically, FOXP3 not only directly upregulated the transcription of GPX4, but also attenuated the degradation of GPX4 mRNA through the linc00857/miR-1290 axis, thereby suppressing ferroptosis and promoting proliferation. Additionally, the FOXP3 inhibitor epirubicin exhibited the ability to impede proliferation and induce ferroptosis in GBM cells both in vitro and in vivo. In summary, our study provided evidences that FOXP3 facilitates the progression of glioblastoma by inhibiting ferroptosis via the linc00857/miR-1290/GPX4 axis, highlighting FOXP3 as a potential therapeutic target for GBM.

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Section: Resultsmentioning

confidence: 99%

FOXP3 promote the progression of glioblastoma via inhibiting ferroptosis mediated by linc00857/miR-1290/GPX4 axis

Cao,

He,

Lan

et al. 2024

Cell Death Dis

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“…Through a ceRNA-mediated mechanism, LINC00857 promotes the growth and invasion of pancreatic cancer cells [ 51 ]. Furthermore, LINC00857 regulates the miR-130b/RHOA axis [ 57 ], which in turn enhances the malignant characteristics of pancreatic cancer. Our findings that LINC00857 is substantially expressed and PAAD patients have a worse prognosis are supported by the aforementioned findings.…”

Section: Discussionmentioning

confidence: 99%

Cuprotosis Programmed-Cell-Death-Related lncRNA Signature Predicts Prognosis and Immune Landscape in PAAD Patients

Chi

Peng

Wang

et al. 2022

Cells

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In terms of mortality and survival, pancreatic cancer is one of the worst malignancies. Known as a unique type of programmed cell death, cuprotosis contributes to tumor cell growth, angiogenesis, and metastasis. Cuprotosis programmed-cell-death-related lncRNAs (CRLs) have been linked to PAAD, although their functions in the tumor microenvironment and prognosis are not well understood. This study included data from the TCGA-PAAD cohort. Random sampling of PAAD data was conducted, splitting the data into two groups for use as a training set and test set (7:3). We searched for differentially expressed genes that were substantially linked to prognosis using univariate Cox and Lasso regression analysis. Through the use of multivariate Cox proportional risk regression, a risk-rating system for prognosis was developed. Correlations between the CRL signature and clinicopathological characteristics, tumor microenvironment, immunotherapy response, and chemotherapy sensitivity were further evaluated. Lastly, qRT-PCR was used to compare CRL expression in healthy tissues to that in tumors. Some CRLs are thought to have strong correlations with PAAD outcomes. These CRLs include AC005332.6, LINC02041, LINC00857, and AL117382.1. The CRL-based signature construction exhibited outstanding predictive performance and offers a fresh approach to evaluating pre-immune effectiveness, paving the way for future studies in precision immuno-oncology.

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“…However, the biological functions of LINC01312 in apoptosis and LUAD have not been systematically analyzed and need to be further investigated. LINC00857 is considered to be an oncogenic lncRNA that promotes proliferation and metastasis of cancer cells in pancreatic ( Chen et al, 2022 ), colorectal ( Chang et al, 2021 ) and breast ( Zheng et al, 2020 ) cancers, and it regulates apoptosis and autophagy ( Su et al, 2020 ). FAM83A.AS1 regulates the proliferation, migration, invasion and epithelial-mesenchymal transition process of LUAD cells by targeting microRNA-141-3p ( Huang et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of a apoptosis-related LncRNA signature to improve prognosis prediction and immunotherapy response in lung adenocarcinoma patients

et al. 2022

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Apoptosis is closely associated with the development of various cancers, including lung adenocarcinoma (LUAD). However, the prognostic value of apoptosis-related lncRNAs (ApoRLs) in LUAD has not been fully elucidated. In the present study, we screened 2, 960 ApoRLs by constructing a co-expression network of mRNAs-lncRNAs associated with apoptosis, and identified 421 ApoRLs that were differentially expressed between LUAD samples and normal lung samples. Sixteen differentially expressed apoptosis-related lncRNAs (DE-ApoRLs) with prognostic relevance to LUAD patients were screened using univariate Cox regression analysis. An apoptosis-related lncRNA signature (ApoRLSig ) containing 10 ApoRLs was constructed by applying the Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression method, and all LUAD patients in the TCGA cohort were divided into high or low risk groups. Moreover, patients in the high-risk group had a worse prognosis (p < 0.05). When analyzed in conjunction with clinical features, we found ApoRLSig to be an independent predictor of LUAD patients and established a prognostic nomogram combining ApoRLSig and clinical features. Gene set enrichment analysis (GSEA) revealed that ApoRLSig is involved in many malignancy-associated immunomodulatory pathways. In addition, there were significant differences in the immune microenvironment and immune cells between the high-risk and low-risk groups. Further analysis revealed that the expression levels of most immune checkpoint genes (ICGs) were higher in the high-risk group, which suggested that the immunotherapy effect was better in the high-risk group than in the low-risk group. And we found that the high-risk group was also better than the low-risk group in terms of chemotherapy effect. In conclusion, we successfully constructed an ApoRLSig which could predict the prognosis of LUAD patients and provide a novel strategy for the antitumor treatment of LUAD patients.

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Long noncoding RNA LINC00857 promotes pancreatic cancer proliferation and metastasis by regulating the miR-130b/RHOA axis

Cited by 14 publications

References 33 publications

FOXP3 promote the progression of glioblastoma via inhibiting ferroptosis mediated by linc00857/miR-1290/GPX4 axis

FOXP3 promote the progression of glioblastoma via inhibiting ferroptosis mediated by linc00857/miR-1290/GPX4 axis

Cuprotosis Programmed-Cell-Death-Related lncRNA Signature Predicts Prognosis and Immune Landscape in PAAD Patients

Identification of a apoptosis-related LncRNA signature to improve prognosis prediction and immunotherapy response in lung adenocarcinoma patients

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