Regulatory Role of the RUNX2 Transcription Factor in Lung Cancer Apoptosis

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dc.contributor.authorBernal, Camila
dc.contributor.authorOtalora, Andrea
dc.contributor.authorCañas, Alejandra
dc.contributor.authorBarreto, Alfonso
dc.contributor.authorPrieto, Karol
dc.contributor.authorMontecino, Martin
dc.contributor.authorRojas, Adriana
dc.date.accessioned2024-09-17T15:55:57Z
dc.date.available2024-09-17T15:55:57Z
dc.date.issued2022
dc.descriptionIndexación: Scopus.
dc.description.abstractLung cancer is the leading cause of cancer death globally. Numerous factors intervene in the onset and progression of lung tumors, among which the participation of lineage-specific transcription factors stands out. Several transcription factors important in embryonic development are abnormally expressed in adult tissues and thus participate in the activation of signaling pathways related to the acquisition of the tumor phenotype. RUNX2 is the transcription factor responsible for osteogenic differentiation in mammals. Current studies have confirmed that RUNX2 is closely related to the proliferation, invasion, and bone metastasis of multiple cancer types, such as osteosarcoma, breast cancer (BC), prostate cancer, gastric cancer, colorectal cancer, and lung cancer. Thus, the present study is aimed at evaluating the role of the RUNX2 transcription factor in inhibiting the apoptosis process. Loss-of-function assays using sh-RNA from lentiviral particles and coupled with Annexin/propidium iodide (PI) assays (flow cytometry), immunofluorescence, and quantitative PCR analysis of genes related to cell apoptosis (BAD, BAX, BCL2, BCL-XL, and MCL1) were performed. Silencing assays and Annexin/PI assays demonstrated that when RUNX2 was absent, the percentage of dead cells increased, and the expression levels of the BCL2, BCL-XL, and MCL1 genes were downregulated. Furthermore, to confirm whether the regulatory role of RUNX2 in the expression of these genes is related to its binding to the promoter region, we performed chromatin immunoprecipitation (ChIP) assays. Here, we report that overexpression of the RUNX2 gene in lung cancer may be related to the inhibition of the intrinsic apoptosis pathway, specifically, through direct transcriptional regulation of the antiapoptotic gene BCL2 and indirect regulation of BCL-XL and MCL1. © 2022 Camila Bernal et al.
dc.description.urihttps://onlinelibrary.wiley.com/doi/10.1155/2022/5198203
dc.identifier.citationInternational Journal of Cell Biology, Volume 2022 2022, Article number 5198203
dc.identifier.doi10.1155/2022/5198203
dc.identifier.issn1687-8876
dc.identifier.urihttps://repositorio.unab.cl/handle/ria/60255
dc.language.isoen
dc.publisherHindawi Limited
dc.rights.licenseAttribution 4.0 International CC BY 4.0 Deed
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAnnexin
dc.subjectBeta actin
dc.subjectDoxorubicin
dc.subjectImmunoglobulin G
dc.subjectMitochondrial protein
dc.subjectPropidium iodide
dc.subjectProtein Bax
dc.subjectProtein bcl 2
dc.subjectProtein bcl xl
dc.subjectProtein mcl 1
dc.subjectShort hairpin RNA
dc.subjectTranscription factor RUNX2
dc.subjectValnivudine
dc.titleRegulatory Role of the RUNX2 Transcription Factor in Lung Cancer Apoptosis
dc.typeArtículo
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