Activation of MYO1G by lncRNA MNX1-AS1 Drives the Progression in Lung Cancer

Lv, Dingding; Wang, Yuhong; Li, Shiyan; Shao, Xiaofeng; Jin, Qinghua

doi:10.1007/s12033-022-00531-y

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…In our study, LINC01132 was screened using GSE98929 and GEPIA to be upregulated in lung cancer, and the elevated level of LINC01132 in the tissues and cells was confirmed by RT-qPCR assay. In the discussion of lncRNAs, evidence suggested that lncRNAs are highly expressed in lung cancer and are regarded as valuable therapeutic factors [ 16 – 18 ]. LINC01132 was also upregulated as a cancer-promoting factor in epithelial ovarian cancer and predicted poor prognosis [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Prognostic significance of LINC01132 in lung cancer and its regulatory role in tumor progression

Hu,

Wei

2024

Discov Onc

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Background The application of long non-coding RNAs (lncRNAs) in cancer has been the focus of research in recent years. This study aimed to discuss the expression and functional mechanism of lncRNA LINC01132 (LINC01132) in lung cancer and explore its prognostic significance in tumors. Methods The expression of LINC01132 in lung cancer patients was verified using GSE98929 screening and real-time quantitative polymerase chain reaction (RT-qPCR) detection. The prognostic potential of LINC01132 was evaluated by performing the chi-square analysis of clinical indicators, Kaplan–Meier analysis, and Cox proportional hazard model. Cell Counting Kit-8 (CCK-8), flow cytometry, and Transwell assay were used to characterize the biological functions of the lung cancer cells. The targeting relationship between LINC01132 and microRNA-125a-3p (miR-125a-3p), miR-125a-3p and SMAD2 was predicted by bioinformatics and verified by luciferase activity assay. Results LINC01132 was upregulated in lung cancer tissues and cells, which was an independent risk factor for survival and prognostic outcomes of lung cancer patients. Silencing LINC01132 suppressed the proliferation and migration of lung cancer cells and accelerated cell death. The target of LINC01132 was miR-125a-3p, and miR-125a-3p inhibitor could eliminate the inhibitory effect of LINC01132 knockdown on the cells. Additionally, SMAD2 is a downstream target of miR-125a-3p, and knockdown of SMAD2 reversed the effects of miR-125a-3p inhibitor on cell migration and invasion. Conclusion LINC01132 may regulate the progression of lung cancer by targeting the miR-125a-3p /SMAD2 axis and serve as a prognostic biomarker for lung cancer.

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Section: Discussionmentioning

confidence: 99%

Prognostic significance of LINC01132 in lung cancer and its regulatory role in tumor progression

Hu,

Wei

2024

Discov Onc

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“…Chu et al showed that miR-96-5p levels were dramatically increased in LC tissues, and its upregulation altered the expression of Bax, MMP9, and Bcl-2 through downregulating domain-binding protein 2, thereby facilitating invasion and proliferation in H1299 cell lines (127). In another study by Lv et al, lncRNA MNX1-AS1 was remarkably increased in LC samples, and its downregulation repressed the proliferation, migration, invasion, and sphere-forming abilities of LC CSCs by activating myosin IG (216). Furthermore, Sun et al revealed that circ_0000376 knockdown decreased PDPK1 levels by releasing miR-545-3p, thereby suppressing NSCLC progression (130).…”

Section: Ncrna In Lc Treatmentmentioning

confidence: 96%

Non-coding RNAs in lung cancer: molecular mechanisms and clinical applications

Liu,

Ding,

Wang

et al. 2023

Front. Oncol.

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Lung cancer (LC) is a heterogeneous disease with high malignant degree, rapid growth, and early metastasis. The clinical outcomes of LC patients are generally poor due to the insufficient elucidation of pathological mechanisms, low efficiency of detection and assessment methods, and lack of individualized therapeutic strategies. Non-coding RNAs (ncRNAs), including microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA), are endogenous regulators that are widely involved in the modulation of almost all aspects of life activities, from organogenesis and aging to immunity and cancer. They commonly play vital roles in various biological processes by regulating gene expression via their interactions with DNA, RNA, or protein. An increasing amount of studies have demonstrated that ncRNAs are closely correlated with the initiation and development of LC. Their dysregulation promotes the progression of LC via distinct mechanisms, such as influencing protein activity, activating oncogenic signaling pathways, or altering specific gene expression. Furthermore, some ncRNAs present certain clinical values as biomarker candidates and therapeutic targets for LC patients. A complete understanding of their mechanisms in LC progression may be highly beneficial to developing ncRNA-based therapeutics for LC patients. This review mainly focuses on the intricate mechanisms of miRNA, lncRNA, and circRNA involved in LC progression and discuss their underlying applications in LC treatment.

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