Corrigendum: The Regulators Associated With N6-Methyladenosine in Lung Adenocarcinoma and Lung Squamous Cell Carcinoma Reveal New Clinical and Prognostic Markers.

[This corrects the article DOI: 10.3389/fcell.2021.741521.].

The Regulators Associated With N6-Methyladenosine in Lung Adenocarcinoma and Lung Squamous Cell Carcinoma Reveal New Clinical and Prognostic Markers.

N6-methyladenosine (m6A) methylation is of significant importance in the initiation and progression of tumors, but how specific genes take effect in different lung cancers still needs to be explored. The aim of this study is to analyze the correlation between the m6A RNA methylation regulators and the occurrence and development of lung cancer. The data of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) were obtained through the TCGA database. We systematically analyzed the related pathological characteristics and prognostic factors by applying univariate and multivariate Cox regression, as well as LASSO Cox regression. Some of 23 m6A regulators are identified as having high expression in lung cancer. In addition, risk score has been shown to be an independent prognostic factor in lung cancer. Our research not only fully reveals that m6A regulators and clinical pathological characteristics are potentially useful with respect to survival and prognosis in different lung tumors but also can lay a theoretical root for the treatment for lung cancer-notably, to point out a new direction for the development of treatment.

Correction: The pan-cancer analysis of the two types of uterine cancer uncovered clinical and prognostic associations with m6A RNA methylation regulators.

Correction for 'The pan-cancer analysis of the two types of uterine cancer uncovered clinical and prognostic associations with m6A RNA methylation regulators' by Zhilin Zou et al., Mol. Omics, 2021, 17, 438-453, DOI: 10.1039/d0mo00113a.

The pan-cancer analysis of the two types of uterine cancer uncovered clinical and prognostic associations with m6A RNA methylation regulators.

The role of m6A RNA methylation modification in uterine cancer has not been studied until now. We explored the relationship between m6A regulators and clinical characteristics and prognosis in uterine corpus endometrial carcinoma (UCEC) and uterine carcinosarcoma (UCS) with the data from the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx). We found that several regulators were up-regulated or down-regulated in the two types of cancer, and identified two cluster subgroups with statistically significant differences in pathological grade, age and survival rate. Multivariate Cox regression analysis showed that methyltransferase-like 16 (METTL16) had a low hazard ratio in UCEC. We used several regulators to construct a risk signature and divided tumor patients into high-risk and low-risk groups, and found that the high-risk group had significantly lower survival rates. Independent prognostic analysis showed that the insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) was a pan-prognostic regulator of uterine cancer. This result was further verified in the Gene Expression Omnibus (GEO) database. Based on above results, we conducted gene-ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to further reveal a potential mechanism for m6A RNA methylation regulators. We found that IGF2BP1 was enriched in gene expression (GO:0010467), poly(A) RNA binding (GO:0044822) and RNA binding (GO:0003723) pathways. KEGG analysis showed that IGF2BP1 was enriched in microRNAs in the cancer (hsa05206) pathway. Our study systematically elucidated the relationship between m6A RNA methylation regulators and uterine cancer and constructed the risk signature that can predict the prognosis and clinicopathological characteristics of uterine cancer.

Clinical and Prognostic Pan-Cancer Analysis of N6-Methyladenosine Regulators in Two Types of Hematological Malignancies: A Retrospective Study Based on TCGA and GTEx Databases.

N6-methyladenosine (m6A) is one of the most active modification factors of mRNA, which is closely related to cell proliferation, differentiation, and tumor development. Here, we explored the relationship between the pathogenesis of hematological malignancies and the clinicopathologic parameters. The datasets of hematological malignancies and controls were obtained from the TCGA [AML (n = 200), DLBCL (n = 48)] and GTEx [whole blood (n = 337), blood vascular artery (n = 606)]. We analyzed the m6A factor expression differences in normal tissue and tumor tissue and their correlations, clustered the express obvious clinical tumor subtypes, determined the tumor risk score, established Cox regression model, performed univariate and multivariate analysis on all datasets. We found that the AML patients with high expression of IGF2BP3, ALKBH5, and IGF2BP2 had poor survival, while the DLBCL patients with high expression of METTL14 had poor survival. In addition, "Total" datasets analysis revealed that IGF2BP1, ALKBH5, IGF2BP2, RBM15, METTL3, and ZNF217 were potential oncogenes for hematologic system tumors. Collectively, the expressions of some m6A regulators are closely related to the occurrence and development of hematologic system tumors, and the intervention of specific regulatory factors may lead to a breakthrough in the treatment in the future.

New insights into molecules and pathways of cancer metabolism and therapeutic implications.

Cancer cells are abnormal cells that can reproduce and regenerate rapidly. They are characterized by unlimited proliferation, transformation and migration, and can destroy normal cells. To meet the needs for cell proliferation and migration, tumor cells acquire molecular materials and energy through unusual metabolic pathways as their metabolism is more vigorous than that of normal cells. Multiple carcinogenic signaling pathways eventually converge to regulate three major metabolic pathways in tumor cells, including glucose, lipid, and amino acid metabolism. The distinct metabolic signatures of cancer cells reflect that metabolic changes are indispensable for the genesis and development of tumor cells. In this review, we report the unique metabolic alterations in tumor cells which occur through various signaling axes, and present various modalities available for cancer diagnosis and clinical therapy. We further provide suggestions for the development of anti-tumor therapeutic drugs.

The cancer exosomes: Clinical implications, applications and challenges.

The exosome is a small functional vesicle enriched in selected proteins, lipids and nucleic acids, displaying distinct molecular heterogeneity. Exosomes released can transform the extracellular matrix microenvironments, transmit signals and molecules to recipient cells and trigger changes in their pathophysiological functions. Tumor-derived exosomes mediate the interactions of tumor cells and microenvironment significantly, and they stimulate tumor growth and development through specific signaling pathways related to metastasis, therapeutic resistance and immunosuppression. Exosome biogenesis from tumors often represents abundant biological information, and novel and efficient isolation and detection methods of exosomes provide a promising approach for tumor diagnosis and prognosis estimation. Moreover, exosome can even be developed as therapeutic agents for multiple disease models based on effective material transport characteristics and biofilm specificity. This review reports the clinical implications and challenges of exosomes in cancer progression, therapy resistance, metastasis and immune escape, and underlying cancerogenic pathological phenotypes including fibrosis and viral infection.