Lnc-TMEM132D-AS1 as a potential therapeutic target for acquired resistance to osimertinib in non-small-cell lung cancer

Wang, Nan; Zhao, Q; Huang, Yutang; Wen, Chunjie; Li, Yaji; Bao, Meihua; Wu, Long‐Fei

doi:10.1039/d2mo00261b

Cited by 6 publications

(2 citation statements)

References 44 publications

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“…For instance, Huang et al discovered that let-7c-5p overexpression arrested cells in G0/G1 phase by targeting cell division cycle 25A, resulting in the repression of proliferation and the promotion of apoptosis in LUAD cells (122). Wang et al revealed that lnc-TMEM132D-AS1 induced M2/G-phase cell cycle arrest, facilitated proliferation, and repressed apoptosis in NSCLC cells by upregulating CD39 via sponging miR-766-5p (123). In addition, circPIM3 was found to increase TNFAIP8 levels by sponging miR-338-3p, thereby repressing apoptosis and promoting cell cycle progress and proliferation in taxol-resistant A549 and PC9 cells (124).…”

Section: Ncrna In Lc Proliferation and Apoptosismentioning

confidence: 99%

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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Section: Ncrna In Lc Proliferation and Apoptosismentioning

confidence: 99%

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

Liu,

Ding,

Wang

et al. 2023

Front. Oncol.

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show abstract

“…In similar ways, it is proved lncRNA human ovarian cancer-specific transcript 2 (HOST2) facilitated gefitinib resistance via functioning as ceRNA for miRNA-621 to upregulate SYF2, a cell cycle-associated protein ( Chen et al, 2019 ). In addition, CCAT1 and lnc-TMEM132D-AS1 were demonstrated to regulate EGFR-TKI resistance in NSCLC through their corresponding ceRNA networks ( Jin et al, 2020 ; Wang et al, 2023 ). This evidence demonstrates the significance of bioinformatics prediction tools for ceRNA networks research.…”

Section: Lncrnas and Other Mechanismsmentioning

confidence: 99%

Long non-coding RNAs in non-small cell lung cancer: implications for EGFR-TKI resistance

Lü

Huang

et al. 2023

Front. Genet.

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Non-small cell lung cancer (NSCLC) is one of the most common types of malignant tumors as well as the leading cause of cancer-related deaths in the world. The application of epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) has dramatically improved the prognosis of NSCLC patients who harbor EGFR mutations. However, despite an excellent initial response, NSCLC inevitably becomes resistant to EGFR-TKIs, leading to irreversible disease progression. Hence, it is of great significance to shed light on the molecular mechanisms underlying the EGFR-TKI resistance in NSCLC. Long non-coding RNAs (lncRNAs) are critical gene modulators that are able to act as oncogenes or tumor suppressors that modulate tumorigenesis, invasion, and metastasis. Recently, extensive evidence demonstrates that lncRNAs also have a significant function in modulating EGFR-TKI resistance in NSCLC. In this review, we present a comprehensive summary of the lncRNAs involved in EGFR-TKI resistance in NSCLC and focus on their detailed mechanisms of action, including activation of alternative bypass signaling pathways, phenotypic transformation, intercellular communication in the tumor microenvironment, competing endogenous RNAs (ceRNAs) networks, and epigenetic modifications. In addition, we briefly discuss the limitations and the clinical implications of current lncRNAs research in this field.

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Silencing of LINC01278 promotes sensitivity of non-small cell lung cancer cells to osimertinib by targeting miR-324-3p/ZFX axis

Lei,

Liu,

Guan

et al. 2024

Cytotechnology

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Lnc-TMEM132D-AS1 as a potential therapeutic target for acquired resistance to osimertinib in non-small-cell lung cancer

Abstract: Acquired resistance is a major obstacle to the therapeutic efficacy of osimertinib in non-small-cell lung cancer (NSCLC). Current knowledge about the role of long non-coding RNAs (lncRNAs) in this phenomenon...

Cited by 6 publications

References 44 publications

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

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

Long non-coding RNAs in non-small cell lung cancer: implications for EGFR-TKI resistance

Silencing of LINC01278 promotes sensitivity of non-small cell lung cancer cells to osimertinib by targeting miR-324-3p/ZFX axis

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