MiR-1-3p targets CENPF to repress tumor-relevant functions of gastric cancer cells

Zhou, Siying; Han, Hui; Yang, Leilei; Lin, Hui Kuan

doi:10.1186/s12876-022-02203-2

Cited by 7 publications

(2 citation statements)

References 24 publications

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“…Tan et al found that C1GALT1 could promote migratory ability and proliferation of BLCA YTS-1 cells in vitro and in vivo, whereas its carcinogenicity was suppressed by miR-1-3p through binding directly to its 3′-untranslated region (3′-UTR) [23]. Zhou et al reported that miR-1-3p negatively mediated CENPF to hamper gastric cancer progression [24]. Du et al suggested that inhibited colorectal cancer cell proliferation and metastasis through suppressing YWHAZ mediated epithelial-mesenchymal transition (EMT) [25].…”

Section: Discussionmentioning

confidence: 99%

GNPNAT1 promotes cancer cells metastasis through stabilization Slug in lung adenocarcinoma

He,

Li,

Jing

et al. 2024

Preprint

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Background Lung cancer is a common malignant tumor with high morbidity and mortality rate. GNPNAT1 has been identified as a metastasis-associated gene in LUAD. However, the exact role and related mechanism of GNPNAT1 in regulating LUAD metastasis remain largely unknown. Method We analyzed the expression of GNPNAT1 in the TIMER2, GEPIA2 and GEO databases and confirmed the results by immunohistochemistry (IHC). The potential biological functions of GNPNAT1 in LUAD was investigated based on TCGA-LUAD database. The correlations between GNPNAT1 and cancer immune characteristics were analyzed via the ESTIMATE and CIBERSORT R package. The underlying mechanisms of altered GNPNAT1 expression on LUAD cell tumorigenesis, proliferation, migration, invasion, and metastasis were explored in vitro and in vivo. Result We demonstrated that GNPNAT1 expression was markedly increased in lung adenocarcinoma (LUAD) tissues and negatively correlated with the overall survival (OS) of patients. hsa − miR − 1−3p and hsa − miR − 26a − 5p were the upstream miRNA targets of GNPNAT1. GNPNAT1 was positively correlated with the infiltration levels of CD8 T cells, memory activated CD4 T cells, NK cells resting, Macrophages M0, Macrophages M1, Neutrophils, gamma delta T cells, Eosinophils, and was negatively correlated with memory resting CD4 T cells, regulatory T cells (Tregs), resting NK cells, Monocytes, resting dendritic cells, resting mast cells. GNPNAT1 knockdown significantly inhibited proliferation, migration, invasion, EMT, and metastasis of LUAD cell, while overexpression of GNPNAT1 revealed the opposite effects. Rescue assay showed that Slug knockdown reversed GNPNAT1-induced LUAD cells migration, invasion, and EMT. Mechanistically, GNPNAT1 promoted cancer cells metastasis via repressing ubiquitination degradation of Slug in LUAD. Conclusion These data indicated that GNPNAT1 was critical for proliferation, migration, invasion, EMT process, and metastasis of LUAD cells and may be a potential therapeutic target for LUAD.

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Section: Discussionmentioning

confidence: 99%

GNPNAT1 promotes cancer cells metastasis through stabilization Slug in lung adenocarcinoma

He,

Li,

Jing

et al. 2024

Preprint

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“…Research has found that miR-1-3p was low expressed in gastric cancer tissues and cells, and was closely related to the size of the tumor. Overexpression of miR-1-3p inhibits the proliferation and invasion of gastric cancer cells by targeting stanniocalcin 2 (STC2) or centromere protein F (CENPF), in which CENPF is also associated with migration [ 56 , 57 ]. Interestingly, miR-1-3p can target glucose-6-phosphate dehydrogenase (G6PD) to affect the Warburg effect (aerobic glycolysis) of gastric cancer cells.…”

Section: Role Of Mir-1-3p In Tumor Occurrence and Developmentmentioning

confidence: 99%

The important role of miR-1-3p in cancers

Dai,

Li,

et al. 2023

J Transl Med

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Cancer is a malignant tumor that seriously threatens human life and health. At present, the main treatment methods include surgical resection, chemotherapy, radiotherapy, and immunotherapy. However, the mechanism of tumor occurrence and development is complex, and it produces resistance to some traditional treatment methods, leading to treatment failure and a high mortality rate for patients. Therefore, exploring the molecular mechanisms of tumor occurrence, development, and drug resistance is a very important task. MiRNAs are a type of non-coding small RNA that regulate a series of biological effects by binding to the 3′-UTR of the target mRNA, degrading the mRNA, or inhibiting its translation. MiR-1-3p is an important member of them, which is abnormally expressed in various tumors and closely related to the occurrence and development of tumors. This article introduces miR-1-3p from multiple aspects, including its production and regulation, role in tumor occurrence and development, clinical significance, role in drug resistance, and approaches for targeting miR-1-3p. Intended to provide readers with a comprehensive understanding of the important role of miR-1-3p in tumors. Graphical Abstract

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miR-1-3p Inhibits Osteosarcoma Cell Proliferation and Cell Cycle Progression While Promoting Cell Apoptosis by Targeting CDK14 to Inactivate Wnt/Beta-Catenin Signaling

et al. 2023

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MiR-1-3p targets CENPF to repress tumor-relevant functions of gastric cancer cells

Cited by 7 publications

References 24 publications

GNPNAT1 promotes cancer cells metastasis through stabilization Slug in lung adenocarcinoma

GNPNAT1 promotes cancer cells metastasis through stabilization Slug in lung adenocarcinoma

The important role of miR-1-3p in cancers

miR-1-3p Inhibits Osteosarcoma Cell Proliferation and Cell Cycle Progression While Promoting Cell Apoptosis by Targeting CDK14 to Inactivate Wnt/Beta-Catenin Signaling

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