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. 2024 Nov 22;24(6):219.
doi: 10.1007/s10142-024-01504-x.

The role of disulfidptosis-associated LncRNA-LINC01137 in Osteosarcoma Biology and its regulatory effects on macrophage polarization

Affiliations

The role of disulfidptosis-associated LncRNA-LINC01137 in Osteosarcoma Biology and its regulatory effects on macrophage polarization

Ning Tang et al. Funct Integr Genomics. .

Abstract

The objective of this research is to investigate the function of long non-coding RNA (lncRNA) associated with disulfidptosis, particularly LINC01137, in osteosarcoma (OS), and its impact on macrophage polarization and the tumor immune microenvironment (TME), with the goal of identifying new prognostic biomarkers and therapeutic targets. Utilizing the OS transcriptome dataset from the TARGET database, differentially expressed lncRNAs related to disulfidptosis were identified. The functional mechanisms of LINC01137, which affect cell proliferation, migration, invasiveness, programmed cell death, and macrophage orientation, were explored using the full suite of analyses provided by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), alongside a diverse array of laboratory experiments, including an in vivo osteosarcoma xenograft model in BALB/c nude mice to assess the impact of LINC01137 knockdown on tumor growth. Among three lncRNAs identified that were distinctly linked to disulfidptosis, LINC01137 showed a notable increase in expression within OS cell lines. Silencing LINC01137 led to a marked decrease in the abilities of cell proliferation, migration, and invasiveness, simultaneously enhancing programmed cell death and facilitating the process of epithelial-mesenchymal transition (EMT). In vivo experiments further confirmed that LINC01137 knockdown significantly suppressed tumor growth in osteosarcoma xenograft models, aligning with the in vitro findings. Associated with disulfidptosis, LINC01137 is pivotal in osteosarcoma development through its enhancement of tumor cell proliferation, migration, and invasiveness, as well as its modification of macrophage orientation within the TME. Given its significance, LINC01137 merits exploration as a prognostic indicator, necessitating detailed studies on its regulatory functions and potential in therapy.

Keywords: Disulfidptosis; LncRNA LINC01137; Macrophage polarization; Osteosarcoma; Tumor immune microenvironment.

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Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests.

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References

    1. Beird HC, Bielack SS, Flanagan AM, et al (2022) Osteosarcoma [published correction appears in Nat Rev Dis Primers. 8(1):82]. Nat Rev Dis Primers. 2022;8(1):77. Published 2022 Dec 8. https://doi.org/10.1038/s41572-022-00409-y
    1. Bian J, Liu Y, Zhao X et al (2023) Research progress in the mechanism and treatment of osteosarcoma. Chin Med J (Engl) 136(20):2412–2420. https://doi.org/10.1097/CM9.0000000000002800 - DOI - PubMed
    1. Cassetta L, Pollard JW (2023) A timeline of tumour-associated macrophage biology. Nat Rev Cancer 23(4):238–257. https://doi.org/10.1038/s41568-022-00547-1 - DOI - PubMed
    1. Cao Y, Wu S, Gu Y, Wong YH, Shi Y, Zhang L (2024) Disulfidptosis-related PABPC3 promotes tumor progression and inhibits immune activity in osteosarcoma. J Gene Med 26(1):e3641. https://doi.org/10.1002/jgm.3641 - DOI - PubMed
    1. Chen P, Shen J (2023) A Disulfidptosis-Related Gene Signature Associated with Prognosis and Immune Cell Infiltration in Osteosarcoma. Bioengineering (Basel). 10(10):1121. https://doi.org/10.3390/bioengineering10101121 . (Published 2023 Sep 25) - DOI - PubMed - PMC

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