Over-expression of lncRNA TMEM161B-AS1 promotes the malignant biological behavior of glioma cells and the resistance to temozolomide via up-regulating the expression of multiple ferroptosis-related genes by sponging hsa-miR-27a-3p

Chen, Qiudan; Wang, Weifeng; Wu, Zhong; Chen, Shuying; Chen, Xiaotong; Zhuang, Shihao; Gao, Song; Yuan, Liang; Yan, Lin

doi:10.1038/s41420-021-00709-4

Cited by 41 publications

(25 citation statements)

References 56 publications

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“…Several lncRNAs were found to be associated with ferroptosis in gliomas. LncRNA TMEM161B-AS1 was identified to promote the malignant behavior and temozolomide resistance through enhancing the expression of multiple ferroptosis-related genes ( 44 ). However, we did not validate the expression of lncRNAs screened by RNA-seq using experimental methods.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane Induces Ferroptosis of Glioma Cells Through Activating the ATF4-CHAC1 Pathway

Zhang

Chen

et al. 2022

Front. Oncol.

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ObjectiveTo clarify the function and mechanisms of sevoflurane (Sev) on ferroptosis in glioma cells.MethodsDifferent concentrations of Sev were used to treat glioma cells U87 and U251. Ferroptosis inducer Erastin was used to incubate glioma cells combined with Sev and ATF4 siRNA transfection treatment. CCK-8 assay and colorimetric assay were performed to analyze cell viability and Fe+ concentration, respectively. The releases of reactive oxygen species (ROS) were determined by flow cytometry analysis. Transcriptional sequencing was used to screen the differential genes affected by Sev in U251 cells. The mRNA and protein expression of ferroptosis-associated genes was detected by qRT-PCR and Western blotting.ResultsSev could suppress cell viability, increase ROS levels and Fe+ concentration, downregulate the protein expression levels of GPX4, and upregulate transferrin, ferritin, and Beclin-1 in a dose-dependent manner in U87 and U251 cells. The expression of ferroptosis and mitophagy-related gene activating transcription factor 4 (ATF4) was identified to be enhanced by Sev analyzed by transcriptional sequencing. ChaC glutathione-specific gamma-glutamylcyclotransferase 1 (CHAC1), which is involved in ferroptosis, is a downstream gene of ATF4. Inhibition of ATF4 could interrupt the expression of CHAC1 induced by Sev in U87 and U251 cells. Ferroptosis inducer Erastin treatment obviously inhibited the cell viability, elevated the Fe2+ concentration, and promoted ROS generation in U87 and U251 cells. The protein level of ATF4 and CHAC1 was increased in Erastin-treated U87 and U251 cells. Moreover, the interruption of Sev-induced ferroptosis and CHAC1 activating induced by ATF4 suppression could be reversed by Erastin.ConclusionsIn summary, this study suggested that Sev exposure-induced ferroptosis by the ATF4-CHAC1 pathway in glioma cells.

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Section: Discussionmentioning

confidence: 99%

Sevoflurane Induces Ferroptosis of Glioma Cells Through Activating the ATF4-CHAC1 Pathway

Zhang

Chen

et al. 2022

Front. Oncol.

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“…Activation of the ferroptosis pathway can induce cancer cell death, especially in the case of drug resistance, and enhance the sensitivity of tumours to chemotherapeutic drugs ( 68 ). Studies have shown that TMZ combined with erastin can significantly improve antitumor activity, which reflects the importance of ferroptosis in the treatment of gliomas ( 31 , 69 , 70 ). Our experiments confirmed that knockdown of PELATON enhanced the sensitivity of GBM cells to erastin and inhibited the proliferation of tumour cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA PELATON, a Ferroptosis Suppressor and Prognositic Signature for GBM

Zhang

et al. 2022

Front. Oncol.

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PELATON is a long noncoding RNA also known as long intergenic nonprotein coding RNA 1272 (LINC01272). The known reports showed that PELATON functions as an onco-lncRNA or a suppressor lncRNA by suppressing miRNA in colorectal cancer, gastric cancer and lung cancer. In this study, we first found that PELATON, as an onco-lncRNA, alleviates the ferroptosis driven by mutant p53 and promotes mutant p53-mediated GBM proliferation. We also first confirmed that PELATON is a new ferroptosis suppressor lncRNA that functions as a ferroptosis inhibitor mainly by mutant P53 mediating the ROS ferroptosis pathway, which inhibits the production of ROS, reduces the levels of divalent iron ions, promotes the expression of SLC7A11, and inhibits the expression of ACSL4 and COX2.PELATON can inhibit the expression of p53 in p53 wild-type GBM cells and regulate the expression of BACH1 and CD44, but it has no effect on p53, BACH1 and CD44 in p53 mutant GBM cells. PELATON and p53 can form a complex through the RNA binding protein EIF4A3. Knockdown of PELATON resulted in smaller mitochondria, increased mitochondrial membrane density, and enhanced sensitivity to ferroptosis inducers to inhibit GBM cell proliferation and invasion. In addition, we established a favourite prognostic model with NCOA4 and PELATON. PELATON is a promising target for the prognosis and treatment of GBM.

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“…The results have been confirmed in other studies. Chen Q. et al (2021) found that lncRNA TMEM161B-AS1 mediated by HSA-Mir-27a-3p had an inhibitory effect on glioma cells, and hsa-Mir-27a-3p inhibited the proliferation, migration, and invasion of glioma cells by down-regulating the expression of FANCD2 and CD44, thus promoting cell apoptosis and ferroptosis. This supports that miR-27a-3p can target TMEM161B-AS1.…”

Section: Discussionmentioning

confidence: 94%

Novel Immune-Related Ferroptosis Signature in Esophageal Cancer: An Informatics Exploration of Biological Processes Related to the TMEM161B-AS1/hsa-miR-27a-3p/GCH1 Regulatory Network

Fan

et al. 2022

Front. Genet.

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Background: Considering the role of immunity and ferroptosis in the invasion, proliferation and treatment of cancer, it is of interest to construct a model of prognostic-related differential expressed immune-related ferroptosis genes (PR-DE-IRFeGs), and explore the ferroptosis-related biological processes in esophageal cancer (ESCA).Methods: Four ESCA datasets were used to identify three PR-DE-IRFeGs for constructing the prognostic model. Validation of our model was based on analyses of internal and external data sets, and comparisons with past models. With the biological-based enrichment analysis as a guide, exploration for ESCA-related biological processes was undertaken with respect to the immune microenvironment, mutations, competing endogenous RNAs (ceRNA), and copy number variation (CNV). The model’s clinical applicability was measured by nomogram and correlation analysis between risk score and gene expression, and also immune-based and chemotherapeutic sensitivity.Results: Three PR-DE-IRFeGs (DDIT3, SLC2A3, and GCH1), risk factors for prognosis of ESCA patients, were the basis for constructing the prognostic model. Validation of our model shows a meaningful capability for prognosis prediction. Furthermore, many biological functions and pathways related to immunity and ferroptosis were enriched in the high-risk group, and the role of the TMEM161B-AS1/hsa-miR-27a-3p/GCH1 network in ESCA is supported. Also, the KMT2D mutation is associated with our risk score and SLC2A3 expression. Overall, the prognostic model was associated with treatment sensitivity and levels of gene expression.Conclusion: A novel, prognostic model was shown to have high predictive value. Biological processes related to immune functions, KMT2D mutation, CNV and the TMEM161B-AS1/hsa-miR-27a-3p/GCH1 network were involved in ESCA progression.

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Over-expression of lncRNA TMEM161B-AS1 promotes the malignant biological behavior of glioma cells and the resistance to temozolomide via up-regulating the expression of multiple ferroptosis-related genes by sponging hsa-miR-27a-3p

Cited by 41 publications

References 56 publications

Sevoflurane Induces Ferroptosis of Glioma Cells Through Activating the ATF4-CHAC1 Pathway

Sevoflurane Induces Ferroptosis of Glioma Cells Through Activating the ATF4-CHAC1 Pathway

LncRNA PELATON, a Ferroptosis Suppressor and Prognositic Signature for GBM

Novel Immune-Related Ferroptosis Signature in Esophageal Cancer: An Informatics Exploration of Biological Processes Related to the TMEM161B-AS1/hsa-miR-27a-3p/GCH1 Regulatory Network

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