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LINC01138表达两种新的异构体，并在胶质瘤细胞中作为一种抑制因子发挥作用。

LINC01138 expresses two novel isoforms and functions as a repressive factor in glioma cells.

作者信息

Zhang Chao, Xu Ao, Liu Ruoyu, Liu Minghang, Zhao Wei, Yao Anhui, Sun Guochen, Ji Shaoping, Zhao Kai

机构信息

Department of Neurosrugery, Tianjin Union Medical Center, Tianjin, 300000, China.

Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475000, China.

出版信息

Heliyon. 2024 Jun 6;10(12):e32245. doi: 10.1016/j.heliyon.2024.e32245. eCollection 2024 Jun 30.

DOI:10.1016/j.heliyon.2024.e32245
PMID:38975094
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11226785/
Abstract

OBJECTIVE

The objective of this study is to investigate the aggressive infiltration of glioblastoma into adjacent brain tissue, considering its challenging prognosis. Initially classified as an intergenic non-coding RNA, we aim to elucidate the functional implications of LINC01138 in glioblastoma.

METHOD

Glioma grading was performed utilizing H&E staining, which unveiled distinct nuclear morphology in high-grade gliomas. The downregulation of LINC01138 in glioma tissues was corroborated through qRT-PCR and gel electrophoresis, concurrently identifying two previously unrecognized LINC01138 isoforms. Expression profiling of all four LINC01138 isoforms was executed in glioma cell lines (A172, SHG-44, U251, U87-MG). The impact of LINC01138 overexpression in U87-MG and U251 cells was evaluated for cell proliferation, migration, and invasion through cell counting, CCK-8 analysis, and Transwell assays. Furthermore, the suppression of LINC01138 in SHG-44 cells substantiated its involvement in fostering tumor malignancy. Transcriptome sequencing revealed the inhibitory influence of LINC01138 on IGF1 expression. These findings contribute to an enriched comprehension of glioma biology by exploring the engagement of LINC01138 through diverse methodologies, thereby elucidating its potential therapeutic significance.

RESULTS

Our investigation elucidates the intricate involvement of LINC01138 in gliomas. High-grade gliomas are characterized by elevated cell density and distinctive nuclear features. LINC01138 demonstrates a substantial downregulation in glioma tissues, with the identification of two novel isoforms. The expression of all four LINC01138 isoforms is notably diminished in both glioma tissues and cell lines. Elevated expression of LINC01138 demonstrates inhibitory effects on tumor cell proliferation, migration, and invasion, while its downregulation exacerbates malignancy. The regulatory function of LINC01138 as a repressor of IGF1 expression was elucidated through transcriptome sequencing.

CONCLUSION

The LINC01138 isoforms display notable tumor-suppressive effects, suggesting a promising potential for impeding glioma progression.

摘要

目的

鉴于胶质母细胞瘤预后不佳，本研究旨在探究其向邻近脑组织的侵袭性浸润情况。最初被归类为基因间非编码RNA，我们旨在阐明LINC01138在胶质母细胞瘤中的功能意义。

方法

利用苏木精-伊红（H&E）染色进行胶质瘤分级，其揭示了高级别胶质瘤中不同的核形态。通过定量逆转录聚合酶链反应（qRT-PCR）和凝胶电泳证实了胶质瘤组织中LINC01138的下调，同时鉴定出两种先前未被识别的LINC01138异构体。在胶质瘤细胞系（A172、SHG-44、U251、U87-MG）中对所有四种LINC01138异构体进行表达谱分析。通过细胞计数、CCK-8分析和Transwell实验评估LINC01138在U87-MG和U251细胞中过表达对细胞增殖、迁移和侵袭的影响。此外，SHG-44细胞中LINC01138的抑制证实了其在促进肿瘤恶性程度方面的作用。转录组测序揭示了LINC01138对胰岛素样生长因子1（IGF1）表达的抑制作用。这些发现通过多种方法探索LINC01138的参与情况，有助于丰富对胶质瘤生物学的理解，从而阐明其潜在的治疗意义。

结果

我们的研究阐明了LINC01138在胶质瘤中的复杂作用。高级别胶质瘤的特征是细胞密度升高和独特的核特征。LINC01138在胶质瘤组织中显著下调，并鉴定出两种新的异构体。所有四种LINC01138异构体在胶质瘤组织和细胞系中的表达均明显降低。LINC01138的高表达对肿瘤细胞增殖、迁移和侵袭具有抑制作用，而其下调则加剧恶性程度。通过转录组测序阐明了LINC01138作为IGF1表达抑制因子的调节功能。

结论

LINC01138异构体显示出显著的肿瘤抑制作用，表明在阻碍胶质瘤进展方面具有潜在的应用前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/26d85c54bf39/mmcfigs14.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/26d85c54bf39/mmcfigs14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/c95e32a7421a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/4329b12c78ae/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/ee59971b80ff/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/09bb221af2d3/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/85c3cad19529/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/298c00a6f50c/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/afa925b026ce/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/c061e1340428/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/070a0f09de08/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/e350822f53f6/mmcfigs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/23c9c8c91fab/mmcfigs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/c8b7f0808775/mmcfigs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/7323bf41ee72/mmcfigs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/8ae628883857/mmcfigs7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/6eb38f513d0d/mmcfigs8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/48db0d8ac45e/mmcfigs9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/de7d34c83ab6/mmcfigs10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/e5bcd36b5ce9/mmcfigs11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/ceed78d14847/mmcfigs12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/d1a9ead32025/mmcfigs13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5028/11226785/26d85c54bf39/mmcfigs14.jpg

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