METTL13 Inhibits Progression of Clear Cell Renal Cell Carcinoma with Repression on PI3K/AKT/mTOR/HIF-1α Pathway and c-Myc Expression

Liu, Zhuonan; Sun, Tianshui; Piao, Chiyuan; Zhang, Zhe; Kong, Chuize

doi:10.21203/rs.3.rs-214061/v1

Cited by 2 publications

(2 citation statements)

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“…3.2 LINC01224 activates the PI3K/AKT/mTOR/HIF-1α axis in GC Activation of the PI3K/AKT/mTOR/HIF-1α axis has an important role in the pathogenesis of numerous cancers [15][16][17] . Thus, we examined the role of LINC01224 on the PI3K/AKT/mTOR/HIF-1α axis in HCG-27 cells by transfecting these cells with si-NC, si-LINC0 1224, oe-NC, or oe-LINC01224.…”

Section: Linc01224 Is Upregulated In Gc Cells and Promotes Gc Develop...mentioning

confidence: 99%

LINC01224 promotes the Warburg effect in gastric cancer by activating the PI3K/AKT/mTOR/HIF-1α axis

Bin,

Liu,

et al. 2023

Preprint

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BACKGROUND: Gastric cancer (GC) is an aggressive malignancy, and patients with advanced-stage GC have high rates of morbidity. The long intergenic non-protein coding RNA 1224 (LINC01224) functions in the pathogenesis of many cancers. We performed in vitro and in vivo studies of the pathogenesis of GC to investigate the effects and mechanism of LINC01224 in this cancer. METHODS: qRT-PCR was used to measure the expression of LINC01224, and qRT-PCR and western blotting were used to measure the expression of genes in the PI3K/AKT/mTOR/HIF-1α axis (phosphoinositide 3-kinase [PI3K], AKT, mammalian target of rapamycin [mTOR], and hypoxia-inducible factor 1 [HIF-1α]) in GC cells. The function of LINC01224 in GC cells was determined using transfection experiments and measurements of cell viability, cell proliferation, colony formation, apoptosis, cell migration, and cell invasion. Glucose metabolism was evaluated using a glucose uptake assay and measurements of lactate. A tumor xenograft model was used to examine the effect of LINC01224 on GC growth in vivo. RESULTS:Up-regulation of LINC01224 in GC cells activated the PI3K/AKT/mTOR/HIF-1α axis and promoted aerobic glycolysis, thereby increasing cell viability, proliferation, migration, and invasion, and decreasing apoptosis. Down-regulation of LINC01224 had the opposite effects. CONCLUSION: LINC01224 promotes the in vitro and in vivo pathogenesis of GC due to upregulation of aerobic glycolysis by activation of the PI3K/AKT/mTOR/HIF-1α axis. These results imply that future studies of GC should examine the effect of targeting of LINC01224 as a treatment strategy.

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Section: Linc01224 Is Upregulated In Gc Cells and Promotes Gc Develop...mentioning

confidence: 99%

LINC01224 promotes the Warburg effect in gastric cancer by activating the PI3K/AKT/mTOR/HIF-1α axis

Bin,

Liu,

et al. 2023

Preprint

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“…Elevated METTL13 expression was related to the favorable prognosis and was beneficial to inhibit tumor growth and metastasis. 11,12 Thus, METTL13 may be a tissue-specific gene and play dual roles in diversified cancers. Nonetheless, to date, the impact of METTL13 on NPC has not yet been elucidated.…”

mentioning

confidence: 99%

METTL13 promotes nasopharyngeal carcinoma progression through regulating the ZEB1/TPT1 axis

Liang

Zhou

et al. 2023

The Journal of Gene Medicine

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Background Globally, nasopharyngeal carcinoma (NPC) is a prevalent and deadly malignancy. Despite the role of methyltransferase like 13 (METTL13) having been highlighted in a majority of human cancers, its function and mechanism in NPC is indistinct. Methods The expression level of METTL13 in NPC cell lines and normal cells was detected using a quantitative real‐time polymerase chain reaction. Gain‐ and loss‐of function experiments were conducted. Cell counting kit‐8, 5‐ethynyl‐2′‐deoxyuridine, wound‐healing, Transwell and tube formation assays, respectively, appraised the proliferative, migratory, invasive and angiogenic cellular responses. Corresponding protein expression was measured by western blotting. A chromatin immunoprecipitation assay was applied to verify the association between ZEB1 and the TPT1 promoter. Eventually, to substantiate the critical role of METTL13 in NPC, the establishment of an in vivo tumorigenesis model was accomplished. Results METTL13 possessed fortified expression in NPC cells. METTL13 silencing markedly suppressed NPC cellular phenotypes in vitro, including proliferative, migratory, invasive and angiogenic events, as well as hindered tumorigenesis in vivo. Additionally, METTL13 positively regulated ZEB1, whereas ZEB1 could bind to TPT1 promoter and transcriptionally regulate TPT1. TPT1 was also found to be upregulated in NPC cells. TPT1 silencing suppressed NPC cellular phenotypes in vitro. TPT1 overexpression partly weakened the anti‐tumor effect of METTL13 in NPC. Conclusions In summary, METTL13 up‐regulated ZEB1, which facilitated the transcriptional activation of TPT1, ultimately promoting NPC growth and metastasis, providing a potential therapeutic strategy for NPC treatment.

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METTL13 Inhibits Progression of Clear Cell Renal Cell Carcinoma with Repression on PI3K/AKT/mTOR/HIF-1α Pathway and c-Myc Expression

Cited by 2 publications

References 44 publications

LINC01224 promotes the Warburg effect in gastric cancer by activating the PI3K/AKT/mTOR/HIF-1α axis

LINC01224 promotes the Warburg effect in gastric cancer by activating the PI3K/AKT/mTOR/HIF-1α axis

METTL13 promotes nasopharyngeal carcinoma progression through regulating the ZEB1/TPT1 axis

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