Signaling pathways governing glioma cancer stem cells behavior

Nasrolahi, Ava; Azizidoost, Shirin; Radoszkiewicz, Klaudia; Najafi, Sajad; Ghaedrahmati, Farhoodeh; Anbiyaee, Omid; Khoshnam, Seyed Esmaeil; Farzaneh, Maryam; Uddin, Shahab

doi:10.1016/j.cellsig.2022.110493

Cited by 22 publications

(10 citation statements)

References 221 publications

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“…In tumor cells, a subpopulation with stem cell characteristics, known as tumor stem cells, exhibits biological features such as self-renewal, multi-lineage differentiation potential, and resistance to conventional treatments [19]. Glioma stem cells induce tumor angiogenesis, promote tumor invasion and spread, display high tolerance to radiotherapy and chemotherapy, and rapidly re-establish tumors under the pressure of conventional treatments, leading to rapid glioma recurrence [20].…”

Section: Discussionmentioning

confidence: 99%

Research progress on function and mechanism of long non-coding RNA in glioma

Feipeng Tai,

Xueming Zhao

2024

Cell Mol Biol (Noisy-le-grand)

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This review aimed to comprehensively summarize the role of long non-coding RNA (lncRNA) in gliomas, the most common malignant tumors in the central nervous system, and explore their potential clinical applications. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a systematic search using the PubMed database was conducted forty studies met the inclusion and exclusion criteria and were analyzed for type of intervention, the study's design, participants' demographics, and outcomes, including attrition. Gliomas, originating within the central nervous system, account for 40-45% of intracranial tumors. Despite advances in neurosurgical techniques, precise radiotherapy, and chemotherapy, the prognosis for glioma patients remains suboptimal. The review highlights the crucial regulatory role of lncRNA in gliomas. Differential expression of various lncRNAs, such as INHEG, SATB2-AS1, PSMB8-AS1, LINC01018, and SPRY4-IT1, has been observed in gliomas, suggesting their involvement in promoting or inhibiting tumorigenesis. Additionally, lncRNAs play roles in glioma characteristics such as proliferation, invasion, migration, angiogenesis, and the presence of glioma stem cells. The potential clinical applications of lncRNA in gliomas involve their association with tumor grading, diameter, metastasis, and family history. This review emphasizes the importance of understanding the molecular mechanisms involving lncRNA in gliomas. The identification of specific lncRNAs associated with gliomas provides potential molecular markers for diagnosis, differentiation, treatment, and prognosis evaluation. Further research is needed to uncover additional key lncRNAs and their underlying mechanisms, ultimately contributing to the improvement of glioma diagnosis and treatment.

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Section: Discussionmentioning

confidence: 99%

Research progress on function and mechanism of long non-coding RNA in glioma

Feipeng Tai,

Xueming Zhao

2024

Cell Mol Biol (Noisy-le-grand)

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“…Moreover, constitutive activation of STAT3 modulates NF-κB signaling and enhances liver cancer stemness [ 45 ]. Simultaneous activation of STAT3 and NF-κB signaling modulates Notch-related genes in GSC [ 46 ]. Since a major cause of chemoresistance is cancer stemness, it is as expected that canonical STAT3 signal transduction pathways play an essential role in cancer stem cell-associated chemoresistance.…”

Section: Discussionmentioning

confidence: 99%

TRPM7 transactivates the FOSL1 gene through STAT3 and enhances glioma stemness

Guo,

Ramar,

Guo

et al. 2023

Cell. Mol. Life Sci.

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Introduction We previously reported that TRPM7 regulates glioma cells’ stemness through STAT3. In addition, we demonstrated that FOSL1 is a response gene for TRPM7, and the FOSL1 gene serves as an oncogene to promote glioma proliferation and invasion. Methods In the present study, we determined the effects of FOSL1 on glioma stem cell (GSC) markers CD133 and ALDH1 by flow cytometry, and the maintenance of stem cell activity by extreme limiting dilution assays (ELDA). To further gain insight into the mechanism by which TRPM7 activates transcription of the FOSL1 gene to contribute to glioma stemness, we constructed a FOSL1 promoter and its GAS mutants followed by luciferase reporter assays and ChIP-qPCR in a glioma cell line and glioma patient-derived xenoline. We further examined GSC markers ALDH1 and TRPM7 as well as FOSL1 by immunohistochemistry staining (IHC) in brain tissue microarray (TMA) of glioma patients. Results We revealed that FOSL1 knockdown reduces the expression of GSC markers CD133 and ALDH1, and FOSL1 is required to maintain stem cell activity in glioma cells. The experiments also showed that mutations of − 328 to − 336 and − 378 to − 386 GAS elements markedly reduced FOSL1 promoter activity. Constitutively active STAT3 increased while dominant-negative STAT3 decreased FOSL1 promoter activity. Furthermore, overexpression of TRPM7 enhanced while silencing of TRPM7 reduced FOSL1 promoter activity. ChIP-qPCR assays revealed that STAT3, present in nuclear lysates of glioma cells stimulated by constitutively activated STAT3, can bind to two GAS elements, respectively. We demonstrated that deacetylation of FOSL1 at the Lys-116 residue located within its DNA binding domain led to an increase in FOSL1 transcriptional activity. We found that the expression of TRPM7, ALDH1, and FOSL1 protein is associated with grades of malignant glioma, and TRPM7 protein expression correlates to the expression of ALDH1 and FOSL1 in glioma patients. Conclusions These combined results demonstrated that TRPM7 induced FOSL1 transcriptional activation, which is mediated by the action of STAT3, a mechanism shown to be important in glioma stemness. These results indicated that FOSL1, similar to GSC markers ALDH1 and TRPM7, is a diagnostic marker and potential drug target for glioma patients.

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“…A novel finding shows an FDA approved PARP1 inhibitor, Niraparib, can inhibit ovarian and PDAC progression through STAT3 inhibition (Zhao et al). We also described the newly discovered BGN/FAP/STAT3 and the Rac1-STAT3 signaling pathways that induce cancer migration and metastasis (4,6,8). What's lacking is how the downstream signaling pathways can integrate the diverse signals, so as to support cancer cell growth and push the progression of neurodegeneration and metabolic disorder.…”

Section: Discussionmentioning

confidence: 99%