circ_0004140 promotes LUAD tumor progression and immune resistance through circ_0004140/miR-1184/CCL22 axis

Liu, Yanyan; Zhang, Haodong; Zhang, Wangli; Xiang, Lanxin; Zhang, Yin; Xu, Hongli; Lü, Ping; Ma, Yifei; Xiong, Lingyi; Zhang, Xiangchen; Liang, Xin; Luo, Jing; Liang, Xinjun

doi:10.1038/s41420-022-00983-w

Cited by 17 publications

(7 citation statements)

References 40 publications

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“…24 Circ_0004140 level was elevated in lung adenocarcinoma, and circ_0004140 interference suppressed lung adenocarcinoma progression via the miR-1184/CCL22. 9 Consistent with this former study, circ_0004140 abundance was found to be enhanced in lung adenocarcinoma. More importantly, circ_0004140 silencing repressed cell proliferation, migration, invasion, and angiogenesis and induced the apoptosis of lung adenocarcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

“…Circ_0000326 expression was markedly upregulated in lung adenocarcinoma, and it contributed to lung adenocarcinoma development via sponging miR‐338‐3p 24 . Circ_0004140 level was elevated in lung adenocarcinoma, and circ_0004140 interference suppressed lung adenocarcinoma progression via the miR‐1184/CCL22 9 . Consistent with this former study, circ_0004140 abundance was found to be enhanced in lung adenocarcinoma.…”

Section: Discussionmentioning

confidence: 99%

“…Circ‐ZNF609 accelerated growth in lung adenocarcinoma via modulating miR‐1224‐3p/ETV1 axis 8 . Notably, a recent report validated that circ_0004140 abundance was enhanced in lung adenocarcinoma, and acted as a carcinogenic factor by boosting cell proliferation and migration in vitro 9 . Yet, the pathogenesis of circ_0004140 involved in lung adenocarcinoma is still largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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Circ_0004140 promotes lung adenocarcinoma progression by upregulating NOVA2 via sponging miR‐330‐5p

Xia,

Xie,

et al. 2023

Thoracic Cancer

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BackgroundCircular RNAs (circRNAs) play a significant role in the tumorigenesis and progression of diverse human cancers, including lung adenocarcinoma. A previous study suggested that circ_0004140 expression was increased in lung adenocarcinoma cells. However, the molecular mechanism of circRNA circ_0004140 involved in lung adenocarcinoma is poorly defined.MethodsCirc_0004140, microRNA‐330‐5p (miR‐330‐5p), and NOVA alternative splicing regulator 2 (NOVA2) expression were determined by real‐time quantitative polymerase chain reaction (RT‐qPCR). Cell proliferation, apoptosis, migration, invasion, and angiogenesis ability were assessed using 5‐ethynyl‐2’‐deoxyuridine (EdU), flow cytometry, wound healing, transwell, and capillary‐like network formation assays. Proliferating cell nuclear antigen (PCNA), cyclin D1, and NOVA2 protein levels were detected using Western blot assay. The interaction between miR‐330‐5p and circ_0004140 or NOVA2 was verified by dual‐luciferase reporter assay. Xenograft tumor model was utilized to assess the role of circ_0004140 in tumor growth in vivo.ResultsCirc_0004140 was upregulated in lung adenocarcinoma tissues and cell lines. Circ_0004140 silencing suppressed cell proliferation, migration, invasion and tube formation ability, and triggered the apoptosis of lung adenocarcinoma cells. Circ_0004140 acted as a molecular sponge for miR‐330‐5p, and miR‐330‐5p silencing largely reversed circ_0004140 knockdown‐induced effects in lung adenocarcinoma cells. NOVA2 was a target of miR‐330‐5p, and NOVA2 overexpression might largely overturn miR‐330‐5p overexpression‐induced influences in lung adenocarcinoma cells. Circ_0004140 upregulated NOVA2 expression via sponging miR‐330‐5p in lung adenocarcinoma cells. Circ_0004140 silencing restrained xenograft tumor growth in vivo.ConclusionCirc_0004140 knockdown might suppress the malignant biological behaviors of lung adenocarcinoma cells via miR‐330‐5p‐dependent regulation of NOVA2.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Circ_0004140 promotes lung adenocarcinoma progression by upregulating NOVA2 via sponging miR‐330‐5p

Xia,

Xie,

et al. 2023

Thoracic Cancer

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“…One of the most studied respiratory diseases is lung cancer, currently one of the most prevalent cancers worldwide 55 . Wang et al.…”

Section: Circrnas Regulate Ferroptosis In Diseasementioning

confidence: 99%

CircRNA and ferroptosis in human disease: Insights for new treatments

Liu,

Zhou,

Cao

2023

Anim Models and Exp Med

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Circular RNA (circRNA), classified as a type of non‐coding RNA, has gained significant attention in the field of biology due to its distinctive ring structure and functional properties. Recent research has provided evidence that specific circRNAs have the ability to modulate disease progression through diverse mechanisms, one of which is by regulating cellular ferroptosis. Ferroptosis is a form of regulated cell death that is driven by iron dependency and lipid peroxidation, and extensive investigations have revealed a relationship between ferroptosis and disease development. In addition to evidence that both circRNAs and ferroptosis exert critical roles in disease progression, circRNAs have also been shown to actively mediate the process of ferroptosis. The relationship between circRNAs and ferroptosis therefore influences disease progression and offers novel targets for disease treatment. By directly or indirectly modulating the expression of circRNAs that regulate the expression of ferroptosis‐related proteins, it may be possible to impact disease progression by promoting or inhibiting ferroptosis. Current research indicates such approaches may hold significant value in a wide variety of common diseases across physiological systems. This review comprehensively summarizes the findings of recent studies investigating the roles of circRNAs in the regulation of ferroptosis in various diseases.

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“…For instance, Jiang et al [3] found that lnc-REG3G-3-1/miR-215-3p facilitates brain metastasis of LUAD via manipulation of Lectin and SLC2A5. Liu et al [4] discovered that circ_0004140/miR-1184/CCL22 axis promotes the progression of LUAD through circ_0004140. In addition, it has been found that sodium selenite weakens the malignant progression of LUAD by inhibiting stemness [5], indicating that inhibiting tumor cell stemness may be one of the strategic approaches to improve the treatment of LUAD.…”

Section: Introductionmentioning

confidence: 99%

Transcription Factor MITF Inhibits the Transcription of CPT1B to Regulate Fatty Acid β-Oxidation and Thus Affects Stemness in Lung Adenocarcinoma Cells

Tang,

et al. 2023

Pharmacology

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Introduction: Cancer stem cells (CSCs) play critical roles in lung adenocarcinoma (LUAD) progression, and fatty acid oxidation is key for CSC growth and survival. Therefore, investigating the molecular mechanisms regulating fatty acid β-oxidation in LUAD is important for its treatment. Methods: Bioinformatics analysis assessed CPT1B and MITF expression and their correlation in LUAD tissues, as well as the pathways enriched by CPT1B. qRT-PCR assessed expression of CPT1B and MITF, while CCK-8 and sphere-forming assays were used to measure cell viability and stemness, respectively. Dual staining detected lipid accumulation, while kits were used to measure fatty acid β-oxidation and glycerol content. qRT-PCR was used to assay expression of lipid oxidation genes. Western blot was used to examine expression of stem cell-related markers. Dual-luciferase assay and ChIP assay were used to verify the binding relationship between MITF and CPT1B. Results: CPT1B was found to be highly expressed in LUAD and enriched in linoleic acid metabolism pathway and α-linolenic acid metabolism pathway. Functional experiments showed that CPT1B could promote stemness in LUAD cells by regulating fatty acid β-oxidation. Additionally, CPT1B was found to be regulated by the upstream transcription factor MITF, which was lowly expressed in LUAD and could downregulate CPT1B expression. Rescue experiments revealed that CPT1B/MITF axis could affect stemness in LUAD cells by regulating fatty acid β-oxidation. Conclusion: Transcription factor MITF inhibited transcription of CPT1B to regulate fatty acid β-oxidation, thereby suppressing stemness in LUAD cells. MITF and CPT1B may become new targets for LUAD.

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circ_0004140 promotes LUAD tumor progression and immune resistance through circ_0004140/miR-1184/CCL22 axis

Cited by 17 publications

References 40 publications

Circ_0004140 promotes lung adenocarcinoma progression by upregulating NOVA2 via sponging miR‐330‐5p

Circ_0004140 promotes lung adenocarcinoma progression by upregulating NOVA2 via sponging miR‐330‐5p

CircRNA and ferroptosis in human disease: Insights for new treatments

Transcription Factor MITF Inhibits the Transcription of CPT1B to Regulate Fatty Acid β-Oxidation and Thus Affects Stemness in Lung Adenocarcinoma Cells

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