Regulatory function of DNA methylation mediated lncRNAs in gastric cancer

Li, Nan; Zeng, Anqi; Wang, Qian; Chen, Maohua; Zhu, Shaomi; Song, Linjiang

doi:10.1186/s12935-022-02648-1

Cited by 19 publications

(14 citation statements)

References 107 publications

(112 reference statements)

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“…29 LncRNAs also play crucial roles in GC progression. 30 It has been shown that lncRNA SNHG3 acts as a tumor-promoting factor in multiple malignancies including GC [31][32][33] but acts as a tumor suppressor in papillary thyroid carcinoma. 34 We herein found that knockdown of METTL3 decreased the m 6 A modification levels of SNHG3, and overexpression of SNHG3 abolished METTL3 knockdownled proliferation inhibition and unveiled poor survival.…”

Section: Discussionmentioning

confidence: 99%

METTL3-mediated m⁶A modification of lncRNA SNHG3 accelerates gastric cancer progression by modulating miR-186-5p/cyclinD2 axis

Ji,

Wang,

2023

Int J Immunopathol Pharmacol

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Objectives METTL3 as an m6A methyltransferase acts in diverse malignancies including gastric cancer (GC). We aimed to reveal the underlying mechanisms by which METTL3 contributes to gastric carcinogenesis. Methods The association of METTL3 and SNHG3 with GC was analyzed by qRT-PCR, Western blot, and TCGA cohort. The functional experiments were implemented to uncover the role of METTL3 in GC. m6A dot blot and MeRIP were used to determine METTL3-mediated m6A modification of lncRNA SNHG3. The effect of METTL3 on SNHG3-mediated miR-186-5p/cyclinD2 axis was evaluated by luciferase gene report, RT-qPCR, and Western blot assays. Results We found that METTL3 was remarkably elevated in GC tissues and correlated with poor survival in patients with GC. Silencing of METTL3 impaired GC cell growth and invasion, whereas restored METTL3 expression promoted these effects. Mechanistically, reduced expression of METTL3 decreased SNHG3 m6A level and caused a decrease in SNHG3 expression, which could further act as a sponge of miR-186-5p to upregulate cyclinD2. Overexpression of SNHG3 attenuated METTL3 knockdown-induced anti-proliferating and miR-186-5p upregulation and cyclinD2 downregulation. Conclusion We find that METTL3-mediated m6A modification of lncRNA SNHG3 accelerates GC progression by modulating miR-186-5p/cyclinD2 axis.

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Section: Discussionmentioning

confidence: 99%

METTL3-mediated m⁶A modification of lncRNA SNHG3 accelerates gastric cancer progression by modulating miR-186-5p/cyclinD2 axis

Ji,

Wang,

2023

Int J Immunopathol Pharmacol

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“…The expression of VEGF is affected by a number of factors, EGF receptor 2, methylation, transforming growth factor (TGF)-α and β, and TNF-α, among which oxygen tension is the most important for pathological angiogenesis (88,89). Hypoxia can rapidly induce VEGF mRNA expression through hypoxia-inducible factor-1 (HIF-1), thus promoting downstream signal transduction (90).…”

Section: Vegf and Inhibition Of The Vegf Pathway In Nsclcmentioning

confidence: 99%

Dual inhibition of EGFR‑VEGF: An effective approach to the treatment of advanced non‑small cell lung cancer with EGFR mutation (Review)

et al. 2023

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On a global scale, the incidence and mortality rates of lung cancer are gradually increasing year by year. A number of bad habits and environmental factors are associated with lung cancer, including smoking, second-hand smoke exposure, occupational exposure, respiratory diseases and genetics. At present, low-dose spiral computed tomography is routinely the first choice in the diagnosis of lung cancer. However, pathological examination is still the gold standard for the diagnosis of lung cancer. Based on the classification and stage of the cancer, treatment options such as surgery, radiotherapy, chemotherapy, targeted therapy and immunotherapy are available. The activation of the EGFR pathway can promote the survival and proliferation of tumor cells, and the VEGF pathway can promote the formation of blood vessels, thereby promoting tumor growth. In non-small cell lung cancer (NSCLC) with EGFR mutation, EGFR activation can promote tumor growth by promoting VEGF upregulation through a hypoxia-independent mechanism. The upregulation of VEGF can make tumor cells resistant to EGFR inhibitors. In addition, the expression of the VEGF signal is also affected by other factors. Therefore, the use of a single EGFR inhibitor cannot completely inhibit the expression of the VEGF signal. In order to overcome this problem, the combination of VEGF inhibitors and EGFR inhibitors has become the method of choice. Dual inhibition can not only overcome the resistance of tumor cells to EGFR inhibitors, but also significantly increase the progression-free survival time of patients with NSCLC. The present review discusses the associations between the EGFR and VEGF pathways, and the characteristics of dual inhibition of the EGFR-VEGF pathway. Contents 1. Introduction 2. Risk factors of lung cancer 3. Diagnosis of NSCLC 4. Treatment of NSCLC 5. EGFR and inhibition of the EGFR pathway in NSCLC 6. VEGF and inhibition of the VEGF pathway in NSCLC 7. Dual-inhibition of EGFR-VEGF 8. Advantages of dual inhibition of EGFR-VEGF 9. Conclusions

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“…Z-ajoene also facilitates β-catenin degradation by regulating CK1α activity (160). Studies using Z-ajoene for the treatment of gastric cancer suggested that the proliferation of MGC-803 gastric cancer cells was considerably inhibited (161,162). Artemisinin is an active sesquiterpene extracted from Artemisia annua.…”

Section: Pnu-74654 Gb1874 and Inhibitor Of B-catenin And Tcf (Icat) P...mentioning

confidence: 99%

Blocking the Wnt/β‑catenin signaling pathway to treat colorectal cancer: Strategies to improve current therapies (Review)

Chen

Deng

2022

Int J Oncol

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Colorectal cancer (CRC) is one of the most common malignant tumor types occurring in the digestive system. The incidence of CRC has exhibits yearly increases and the mortality rate among patients with CRC is high. The Wnt/β-catenin signaling pathway, which is associated with carcinogenesis, is abnormally activated in CRC. Most patients with CRC have adenomatous polyposis coli mutations, while half of the remaining patients have β-catenin gene mutations. Therefore, targeting the Wnt/β-catenin signaling pathway for the treatment of CRC is of clinical value. In recent years, with in-depth research on the Wnt/β-catenin signaling pathway, inhibitors have been developed that are able to suppress or hinder the development and progression of CRC. In the present review, the role of the Wnt/β-catenin signaling pathway in CRC is summarized, the research status on Wnt/β-catenin pathway inhibitors is outlined and potential targets for inhibition of this pathway are presented. Contents 1. Introduction 2. Current status of CRC treatments 3. Overview of the Wnt signaling pathway 4. Role of the Wnt/β-catenin signaling pathway in the development and progression of CRC 5.

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Regulatory function of DNA methylation mediated lncRNAs in gastric cancer

Cited by 19 publications

References 107 publications

METTL3-mediated m⁶A modification of lncRNA SNHG3 accelerates gastric cancer progression by modulating miR-186-5p/cyclinD2 axis

METTL3-mediated m⁶A modification of lncRNA SNHG3 accelerates gastric cancer progression by modulating miR-186-5p/cyclinD2 axis

Dual inhibition of EGFR‑VEGF: An effective approach to the treatment of advanced non‑small cell lung cancer with EGFR mutation (Review)

Blocking the Wnt/β‑catenin signaling pathway to treat colorectal cancer: Strategies to improve current therapies (Review)

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Regulatory function of DNA methylation mediated lncRNAs in gastric cancer

Cited by 19 publications

References 107 publications

METTL3-mediated m6A modification of lncRNA SNHG3 accelerates gastric cancer progression by modulating miR-186-5p/cyclinD2 axis

METTL3-mediated m6A modification of lncRNA SNHG3 accelerates gastric cancer progression by modulating miR-186-5p/cyclinD2 axis

Dual inhibition of EGFR‑VEGF: An effective approach to the treatment of advanced non‑small cell lung cancer with EGFR mutation (Review)

Blocking the Wnt/β‑catenin signaling pathway to treat colorectal cancer: Strategies to improve current therapies (Review)

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METTL3-mediated m⁶A modification of lncRNA SNHG3 accelerates gastric cancer progression by modulating miR-186-5p/cyclinD2 axis

METTL3-mediated m⁶A modification of lncRNA SNHG3 accelerates gastric cancer progression by modulating miR-186-5p/cyclinD2 axis