METTL13 facilitates cell growth and metastasis in gastric cancer via an eEF1A/HN1L positive feedback circuit

Wu, Qiong; Hu, Qingqing; Hai, Yanan; Li, Yandong; Gao, Yong

doi:10.1007/s12079-022-00687-x

Cited by 11 publications

(8 citation statements)

References 38 publications

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“…Previously, METTL13 expression was markedly raised, and an absence of METTL13 greatly inhibited proliferation at the same time as it potentiated apoptosis in vitro, and hindered tumor growth in vivo in head and neck squamous cell carcinoma 8 . In addition, METTL13 overexpression drove cell growth and migration in gastric cancer 10 . Consistently, we also noted an abnormal upregulation of METTL13 in NPC cells.…”

Section: Discussionsupporting

confidence: 84%

“…8 In addition, METTL13 overexpression drove cell growth and migration in gastric cancer. 10 Consistently, we also noted an abnormal upregulation of METTL13 in NPC cells. METTL13 knockdown not only disturbed NPC cell proliferation, migration and invasion along with angiogenesis, but also retarded tumor growth.…”

Section: Discussionsupporting

confidence: 80%

“…7 Recent studies revealed that METTL13 was dysregulated in several types of cancer and influenced tumorigenesis and progression. An upregulated level of METTL13 was discovered not only to be negatively associated with clinical prognosis, but also to drive cancer cell malignant phenotypes and facilitate cancer development and metastasis, functioning as an oncogenic role [8][9][10] ; on the contrary, METTL13 was reported to be lowly expressed and served as an anti-oncogene in bladder carcinoma and clear cell renal cell cancer. Elevated METTL13 expression was related to the favorable prognosis and was beneficial to inhibit tumor growth and metastasis.…”

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confidence: 99%

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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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Section: Discussionsupporting

confidence: 84%

Section: Discussionsupporting

confidence: 80%

mentioning

confidence: 99%

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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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“…This study underscores the critical role of cell elongation and morphological changes in the migration, growth, and metastasis of cancer cells, as highlighted in previous research [22,23]. Speci cally, ADSCs have been reported to facilitate the EMT in various cancers, including lung and pancreatic cancers [24,25].…”

Section: Verifying Interaction With Breast Cancer Cells and Adscs Thr...supporting

confidence: 68%

3D spheroid model of adipose-derived stem cell and breast cancer cell co- culture for mimicking cell migration and the cancer environment

Kim,

Bae

et al. 2023

Preprint

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Traditional two-dimensional (2D) cell culture methodologies exhibit significant limitations, notably their failure to replicate the intricate three-dimensional (3D) milieu of human tissue architecture. This discrepancy has catalyzed the exploration of advanced drug screening platforms that more faithfully mimic the complex 3D biological environment. To this end, precision medicine research has increasingly used 3D in vitro models that emulate the tissue microenvironment of the human body. In this study, breast cancer cell lines (MDA-MB-231 and SK-BR-3) were co-cultured with adipose-derived stem cells (ADSCs), mimicking the in vitro 3D tumor microenvironment with the multicellular and heterogeneous nature of solid tumors compared to a 2D cancer cell only system. Additionally, collagen type I was used to replicate the microenvironment within a 3D spheroid platform, enhancing the accuracy of the platform in mimicking human tissue characteristics. Significantly, the interactions between the ADSCs and two breast cancer lines markedly influenced factors such as cell elongation, molecular expression, migration patterns, and drug sensitivity. The integration of ADSCs was pivotal in simulating the cancer microenvironment, highlighting that even within the same cancer cell line, varying microenvironmental contexts can lead to vastly different experimental results. Thus, this study provides insights into the role of factors such as cellular substrates and stem cells in simulating a 3D tumor microenvironment more akin to the human body when constructing a 3D in vitro system based on breast cancer cells.

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“…An intriguing aspect of this research is the observed interaction between EEF1A2 and HSPB8, where EEF1A2 serves to positively regulate the expression of HSPB8 [ 47 ]. A pivotal role for EEF1A2 emerged in a recent study in gastric cancer revealed that METTL13, which is linked to cancers in humans, works together with EEF1A2 in a loop that causes abnormal levels of the cancer-promoting gene HN1L [ 48 ]. Interestingly, the results from the TCGA dataset (STAD) for stomach adenocarcinoma showed a significant decrease in EEF1A2 expression compared with adjacent normal tissue and GTEx normal samples (Fig.…”

Section: Eef1a2 Switching On In Tumorigenesismentioning

confidence: 99%

Oncogenic activation of EEF1A2 expression: a journey from a putative to an established oncogene

Patel,

Hassan,

Dixit

2024

Cell Mol Biol Lett

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Protein synthesis via translation is a central process involving several essential proteins called translation factors. Although traditionally described as cellular “housekeepers,” multiple studies have now supported that protein initiation and elongation factors regulate cell growth, apoptosis, and tumorigenesis. One such translation factor is eukaryotic elongation factor 1 alpha 2 (EEF1A2), a member of the eukaryotic elongation factor family, which has a canonical role in the delivery of aminoacyl-tRNA to the A-site of the ribosome in a guanosine 5′-triphosphate (GTP)-dependent manner. EEF1A2 differs from its closely related isoform, EEF1A1, in tissue distribution. While EEF1A1 is present ubiquitously, EEF1A2 replaces it in specialized tissues. The reason why certain specialized tissues need to essentially switch EEF1A1 expression altogether with EEF1A2 remains to be answered. Abnormal “switch on” of the EEF1A2 gene in normal tissues is witnessed and is seen as a cause of oncogenic transformation in a wide variety of solid tumors. This review presents the journey of finding increased expression of EEF1A2 in multiple cancers, establishing molecular mechanism, and exploring it as a target for cancer therapy. More precisely, we have compiled studies in seven types of cancers that have reported EEF1A2 overexpression. We have discussed the effect of aberrant EEF1A2 expression on the oncogenic properties of cells, signaling pathways, and interacting partners of EEF1A2. More importantly, in the last part, we have discussed the unique potential of EEF1A2 as a therapeutic target. This review article gives an up-to-date account of EEF1A2 as an oncogene and can draw the attention of the scientific community, attracting more research.

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METTL13 facilitates cell growth and metastasis in gastric cancer via an eEF1A/HN1L positive feedback circuit

Cited by 11 publications

References 38 publications

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

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

3D spheroid model of adipose-derived stem cell and breast cancer cell co- culture for mimicking cell migration and the cancer environment

Oncogenic activation of EEF1A2 expression: a journey from a putative to an established oncogene

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