CircZBTB44 promotes renal carcinoma progression by stabilizing HK3 mRNA structure

Li, Tushuai; Gu, Yue; Xu, Bin; Kuča, Kamil; Zhang, Jie; Wu, Wei

doi:10.1186/s12943-023-01771-5

Cited by 8 publications

(2 citation statements)

References 49 publications

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“…Major m6A methylase (Chen, Gong, et al, 2022) METTL14 Enhance the catalytic ability of mettl3 and recognize substrates (Liu, Du, et al, 2022) WTAP Regulating the recruitment of MTC to mRNA targets (Ping et al, 2014) METTL16 Catalytic methylation of U6-snRNA (Ruszkowska, 2021) METTL5 Catalytic methylation of 18S rRNA (van Tran et al, 2019) Eraser FTO Remove m6A methylation (Su et al, 2020) ALKBH5 Remove m6A methylation Reader -YTHDC1 promote pre-mRNA splicing, RNA nuclear export, mRNA degradation (Roundtree, Luo, et al, 2017;Xiao, Adhikari, et al, 2016;Zhang, Wang, et al, 2020) YTHDC2 promote mRNA translation and degradation (Ma et al, 2021;Yuan et al, 2022) YTHDF1 promote mRNA translation (Wang et al, 2015) YTHDF2 promote mRNA degradation (Wang et al, 2014) YTHDF3 affect mRNA translation and degradation by interacting with YTHDF1 or YTHDF2 (Shi et al, 2017) HNRNPA2B1 promote the processing of pri-miRNA and splicing of specific mRNA (Alarcón et al, 2015) HNRNPG affect splicing of certain precursor mRNA (Zhou et al, 2019) HNRNPC affect mRNA stability and nuclear export (Li, Gu, et al, 2023;Liu, Luo, et al, 2022) IGF2BP1/2/3 promote the stability and translation of mRNA (Huang et al, 2018) TAO ET AL.…”

Section: Mettl3mentioning

confidence: 99%

M6A methylation‐regulated autophagy may be a new therapeutic target for intervertebral disc degeneration

Tao,

Yu,

et al. 2024

Cell Biology International

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Degeneration of intervertebral discs is considered one of the most important causes of low back pain and disability. The intervertebral disc (IVD) is characterized by its susceptibility to various stressors that accelerate the senescence and apoptosis of nucleus pulposus cells, resulting in the loss of these cells and dysfunction of the intervertebral disc. Therefore, how to reduce the loss of nucleus pulposus cells under stress environment is the main problem in treating intervertebral disc degeneration. Autophagy is a kind of programmed cell death, which can provide energy by recycling substances in cells. It is considered to be an effective method to reduce the senescence and apoptosis of nucleus pulposus cells under stress. However, further research is needed on the mechanisms by which autophagy of nucleus pulposus cells is regulated under stress environments. M6A methylation, as the most extensive RNA modification in eukaryotic cells, participates in various cellular biological functions and is believed to be related to the regulation of autophagy under stress environments, may play a significant role in nucleus pulposus responding to stress. This article first summarizes the effects of various stressors on the death and autophagy of nucleus pulposus cells. Then, it summarizes the regulatory mechanism of m6A methylation on autophagy‐related genes under stress and the role of these autophagy genes in nucleus pulposus cells. Finally, it proposes that the methylation modification of autophagy‐related genes regulated by m6A may become a new treatment approach for intervertebral disc degeneration, providing new insights and ideas for the clinical treatment of intervertebral disc degeneration.

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Section: Mettl3mentioning

confidence: 99%

M6A methylation‐regulated autophagy may be a new therapeutic target for intervertebral disc degeneration

Tao,

Yu,

et al. 2024

Cell Biology International

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“…Recent studies have shown significant upregulation of HK1 and HK2 in various malignant tumors, such as breast, colon, thyroid, and kidney cancers [18]. These enzymes regulate the glycolytic pathway, contributing to unfavorable prognostic outcomes [19,20]. In colorectal cancer cell lines, HK1 and HK2 are dynamically regulated through feedback mechanisms [17].…”

Section: Introductionmentioning

confidence: 99%

Dual roles of HK3 in regulating the network between tumor cells and tumor-associated macrophages in neuroblastoma

Wu,

Mi,

Jin

et al. 2024

Cancer Immunol Immunother

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Neuroblastoma (NB) is the most common and deadliest extracranial solid tumor in children. Targeting tumor-associated macrophages (TAMs) is a strategy for attenuating tumor-promoting states. The crosstalk between cancer cells and TAMs plays a pivotal role in mediating tumor progression in NB. The overexpression of Hexokinase-3 (HK3), a pivotal enzyme in glucose metabolism, has been associated with poor prognosis in NB patients. Furthermore, it correlates with the infiltration of M2-like macrophages within NB tumors, indicating its significant involvement in tumor progression. Therefore, HK3 not only directly regulates the malignant biological behaviors of tumor cells, such as proliferation, migration, and invasion, but also recruits and polarizes M2-like macrophages through the PI3K/AKT-CXCL14 axis in neuroblastoma. The secretion of lactate and histone lactylation alterations within tumor cells accompanies this interaction. Additionally, elevated expression of HK3 in M2-TAMs was found at the same time. Modulating HK3 within M2-TAMs alters the biological behavior of tumor cells, as demonstrated by our in vitro studies. This study highlights the pivotal role of HK3 in the progression of NB malignancy and its intricate regulatory network with M2-TAMs. It establishes HK3 as a promising dual-functional biomarker and therapeutic target in combating neuroblastoma.

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Inducing disulfidptosis in tumors:potential pathways and significance

Mi,

Kong,

Chen

et al. 2024

MedComm

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Regulated cell death (RCD) is crucial for the elimination of abnormal cells. In recent years, strategies aimed at inducing RCD, particularly apoptosis, have become increasingly important in cancer therapy. However, the ability of tumor cells to evade apoptosis has led to treatment resistance and relapse, prompting extensive research into alternative death processes in cancer cells. A recent study identified a novel form of RCD known as disulfidptosis, which is linked to disulfide stress. Cancer cells import cystine from the extracellular environment via solute carrier family 7 member 11 (SLC7A11) and convert it to cysteine using nicotinamide adenine dinucleotide phosphate (NADPH). When NADPH is deficient or its utilization is impaired, cystine accumulates, leading to the formation of disulfide bonds in the actin cytoskeleton, triggering disulfidptosis. Disulfidptosis reveals a metabolic vulnerability in tumors, offering new insights into cancer therapy strategies. This review provides a detailed overview of the mechanisms underlying disulfidptosis, the current research progress, and limitations. It also highlights innovative strategies for inducing disulfidptosis and explores the potential of combining these approaches with traditional cancer therapies, particularly immunotherapy, to expedite clinical translation.

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CircZBTB44 promotes renal carcinoma progression by stabilizing HK3 mRNA structure

Cited by 8 publications

References 49 publications

M6A methylation‐regulated autophagy may be a new therapeutic target for intervertebral disc degeneration

M6A methylation‐regulated autophagy may be a new therapeutic target for intervertebral disc degeneration

Dual roles of HK3 in regulating the network between tumor cells and tumor-associated macrophages in neuroblastoma

Inducing disulfidptosis in tumors:potential pathways and significance

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