Ru^II-Catalyzed/NH₂‑Assisted Selective Alkenyl C–H [5 + 1] Annulation of Alkenylanilines with Sulfoxonium Ylides to Quinolines

A novel ruthenium-catalyzed [5 + 1] annulation of 2-alkenylanilines with sulfoxonium ylides was developed for the rapid assembly of highly functionalized quinolines. This new catalytic process employs challenging but synthetically ideal free amino functionality to achieve alkenyl C–H activation with sulfoxonium ylides as one-carbon coupling partners. Various 2-acylquinolines could be obtained with good yields and excellent functional group tolerance. Moreover, the potential synthetic application of this methodology was exemplified by several chemical transformations

Image13_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).TIF

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p

Image9_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).TIF

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p

Image4_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).TIF

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p

DataSheet2_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).PDF

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p

Image2_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).TIF

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p

Image7_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).TIF

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p

Table1_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).DOCX

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p

Image14_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).TIF

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p

Image11_Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).TIF

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.</p