Publications by authors named "Huiran Lin"

Background: Heterogeneous clinical features and prognosis in neuroblastoma (NB) children are frequently dominated by immune elements. Dysfunction and apoptosis in immune cells result from the exposure to continuous tumor-related antigen stimulation and coinhibitory signals. To date, key factors pointing to the restriction of NB-specific CD8 T cells remain elusive.

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-acetyltransferase 10 (NAT10) is a nucleolar acetyltransferase with an acetylation catalytic function and can bind various protein and RNA molecules. As the N4-acetylcytidine (ac4C) "writer" enzyme, NAT10 is reportedly involved in a variety of physiological and pathological activities. Currently, the NAT10-related molecular mechanisms in various cancers are not fully understood.

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Neuroblastoma (NB), a rare childhood cancer originating in nerve tissue. YTHDF3, a member of the YTH domain protein family, is involved in RNA m6A modification and cancer progression. Polymorphisms in YTHDF3 may influence its expression and biological function.

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Article Synopsis
  • Neuroblastoma (NB) is a common childhood cancer, and variations in the METTL1/WDR4 genes may indicate risk for developing this disease.
  • Researchers analyzed genetic data from 898 NB patients and 1734 healthy controls to explore the link between METTL1/WDR4 gene polymorphisms and NB susceptibility.
  • While individual SNPs didn’t show strong associations, having a combination of protective WDR4 genotypes was linked to a reduced risk of NB, suggesting that these genetic variations could serve as biomarkers for identifying at-risk populations.
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Objective: Neuroblastoma is a life-threatening pediatric solid tumor whose etiology remains unclear. N7-methylguanosine (m7G) is one of the most important epigenetic modifications of RNA, which plays a crucial role in tumorigenesis. The m7G-mediated genes and also have been reported to be dysregulated in various cancers.

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Objective: AlkB homolog 5 (ALKBH5) has been proven to be closely related to tumors. However, the role and molecular mechanism of ALKBH5 in neuroblastomas have rarely been reported.

Methods: The potential functional single-nucleotide polymorphisms (SNPs) in were identified by National Center for Biotechnology Information (NCBI) dbSNP screening and SNPinfo software.

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The recurrence and metastasis of children with mediastinal neuroblastoma (NB) are also occurred after surgery, chemotherapy, or radiotherapy. Strategies targeting the tumor microenvironment have been reported to improve survival; however, thorough investigations of monocytes and tumor-associated macrophages (Mϕs) with specialized functions in NB are still lacking. Our data first demonstrated polypyrimidine tract binding protein 2 (PTBP2) as a possible identifier in patients with mediastinal NB screened by proteomic profiling and that PTBP2 predicted good outcomes.

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N7-methylguanosine (mG) is a significant RNA modification occurring during epigenetic regulation. An increasing number of investigations have proved that the effect of mG in suppressing cancer deserves more attention. Herein, we explore potential valuable targets based on present studies of mG-related cancer to improve disease therapy and prognoses.

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Objective: Gliomas are the most common tumors in the central nervous system. The cancer susceptibility candidate 15 (CASC15) gene has been reported to be a susceptibility gene for several types of cancer. No studies have been carried out on the predisposing effect of CASC15 gene single nucleotide polymorphisms (SNPs) on glioma risk.

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Background: Glioma is one of the central nervous system (CNS) tumors in children, accounting for 80% of malignant brain tumors. Nucleotide excision repair (NER) is a vital pathway during DNA damage repair progression. Xeroderma pigmentosum group D (XPD) or excision repair cross-complementing group 2 (ERCC2) is a critical factor in the NER pathway, playing an indispensable role in the DNA repair process.

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It is well known that noncoding RNAs (ncRNAs) cannot encode proteins, but they can play important regulatory roles in tumors by combining with proteins, RNAs, and DNAs. As more and more studies reveal the important roles and underlying mechanisms of long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) in cancer, their huge application potential in cancer therapy cannot be ignored. For example, lncRNAs can be involved in tumor-related signal transduction pathways, cell cycle control, DNA damage, epigenetic regulation, and microRNA control.

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Introduction: Central nervous system (CNS) tumors comprise 15-20% of all malignancies occurring in childhood and adolescence. Previous researches have shown that overexpression and amplification of the AURKA gene could induce multiple human malignancies, with which the connection of CNS tumor susceptibility has not been extensively studied.

Material And Methods: In this study, we assessed whether and to what extent AURKA gene single nucleotide polymorphisms (SNPs) (rs1047972 C > T, rs2273535 T > A, rs8173 G > C) were associated with CNS tumor susceptibility, based on a case-control analysis in 191 CNS tumor patients and 248 controls.

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With the development of RNA modification research, the importance of N6-methyladenosine (m6A) in tumors cannot be ignored. m6A promotes the self-renewal of tumor stem cells and the proliferation of tumor cells. It affects post-transcriptional gene expression through epigenetic mechanisms, combining various factors to determine proteins' fate and altering the biological function.

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RNA modification plays a crucial role in many biological functions, and its abnormal regulation is associated with the progression of cancer. Among them, N-methyladenine (mA) is the most abundant RNA modification. Methyltransferase-like 14 (METTL14) is the central component of the mA methylated transferase complex, which is involved in the dynamic reversible process of mA modification.

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Importance: LIM domain only 1 () gene polymorphisms were previously found to be implicated in the risk of several cancers. No available studies were performed regarding the predisposing effect of gene single nucleotide polymorphisms (SNPs) on central nervous system (CNS) tumor risk.

Objective: We aimed to determine whether the gene SNPs were associated with the risk of CNS tumor by applying a case-control study with 191 cases and 248 controls in China.

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Neuroblastoma is a common solid tumor in children and a leading cause of cancer death in children. Neuroblastoma exhibits genetic, morphological, and clinical heterogeneity that limits the efficacy of current monotherapies. With further research on neuroblastoma, the pathogenesis of neuroblastoma is found to be complex, and more and more treatment therapies are needed.

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Background: Wilms tumor is a highly heritable malignancy. Aberrant METTL14, a critical component of N6-methyladenosine (mA) methyltransferase, is involved in carcinogenesis. The association between genetic variants in the METTL14 gene and Wilms tumor susceptibility remains to be fully elucidated.

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Gliomas are the most prevalent brain tumors among children and adolescents. The occurrence and development of various malignant tumors is closely related with gene, but its relationship with glioma susceptibility has not been widely discovered. In this case-control study, we conducted four single nucleotide polymorphisms (SNPs) (rs3811464 G>A, rs3811463 T>C, rs34787247 G>A, and rs11247957 G>A) of gene to investigate whether they increase the risk of glioma.

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Background: Wilms tumor is the most frequent renal malignancy in children. YTHDF1 is associated with the development of several kinds of cancers, yet whether common variants of the YTHDF1 gene influence Wilms tumor risk is unknown. We present, here, a hospital-based case-control study specifically designed to investigate the role of YTHDF1 genetic variants on Wilms tumor.

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Background: Glioma, also known as neuroglioma, is the most common primary tumors of the central nervous system. Many previous studies have reported associations between RAS gene polymorphisms and multiple tumors. However, the role of RAS gene polymorphisms on glioma risk has not been investigated.

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Glioma is a highly heritable disease with a strong genetic component. The N6-methyladenosine (mA) modification core genes play important roles in the context of cancer. However, the effects of polymorphisms in the mA modification core genes on the risk of pediatric glioma remain undefined.

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Due to its high proliferation capacity and rapid intracranial spread, glioblastoma (GBM) has become one of the least curable malignant cancers. Recently, the competing endogenous RNAs (ceRNAs) hypothesis has become a focus in the researches of molecular biological mechanisms of cancer occurrence and progression. However, there is a lack of correlation studies on GBM, as well as a lack of comprehensive analyses of GBM molecular mechanisms based on high-throughput sequencing and large-scale sample sizes.

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Recent studies have revealed that long non-coding RNAs (lncRNAs) play critical roles in the tumorigenesis and proliferation of human cancer. Several polymorphisms of lncRNAs have been found to be involved in the risk of neuroblastoma (NB). However, studies on the relationship between polymorphisms in lncRNA exons and NB are infrequent.

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