Supplementary Tables from The IGF2BP3–COPS7B Axis Facilitates mRNA Translation to Drive Colorectal Cancer Progression

Supplementary Tables from The IGF2BP3–COPS7B Axis Facilitates mRNA Translation to Drive Colorectal Cancer Progression

<p>Supplementary Tables</p>

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Bibliografiske detaljer
Hovedforfatter:	Jing Tang (17314958) (author)
Andre forfattere:	Shuoshuo Wang (17314961) (author), Mingjiao Weng (17314964) (author), Qingyu Guo (17314967) (author), Lili Ren (17314970) (author), Yan He (17314973) (author), Zihan Cui (17314976) (author), Mingqi Cong (17314979) (author), Minglu Qin (17314982) (author), Jia Yu (11566524) (author), Rui Su (17314985) (author), Xiaobo Li (17314988) (author)
Udgivet:	2025
Fag:	Cancer Cancer Biology Tumor Biology Molecular and Cellular Biology Carcinogenesis Gastrointestinal Cancers Colorectal cancer Gene Regulation Posttranscriptional and translational control Oncogenes & Tumor Suppressors Oncogenes Progression, Invasion & Metastasis Tumor progression
Tags:	Tilføj Tag Ingen Tags, Vær først til at tagge denne postø!

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Table S2 from An <i>In Vivo</i> CRISPR Screen Identifies That SNRPC Promotes Triple-Negative Breast Cancer Progression
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Table S3 from An <i>In Vivo</i> CRISPR Screen Identifies That SNRPC Promotes Triple-Negative Breast Cancer Progression
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Table S7 from An <i>In Vivo</i> CRISPR Screen Identifies That SNRPC Promotes Triple-Negative Breast Cancer Progression
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Table S8 from An <i>In Vivo</i> CRISPR Screen Identifies That SNRPC Promotes Triple-Negative Breast Cancer Progression
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Supplementary Table S3 from The Polyamine–Hypusine Circuit Controls an Oncogenic Translational Program Essential for Malignant Conversion in MYC-Driven Lymphoma
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Supplementary Table S4 from The Polyamine–Hypusine Circuit Controls an Oncogenic Translational Program Essential for Malignant Conversion in MYC-Driven Lymphoma
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Table S2 from MEX3A Mediates p53 Degradation to Suppress Ferroptosis and Facilitate Ovarian Cancer Tumorigenesis
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Supplementary table S2 from SMAD4 Loss Induces c-MYC–Mediated NLE1 Upregulation to Support Protein Biosynthesis, Colorectal Cancer Growth, and Metastasis
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Supplementary table S3 from SMAD4 Loss Induces c-MYC–Mediated NLE1 Upregulation to Support Protein Biosynthesis, Colorectal Cancer Growth, and Metastasis
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Supplementary table S4 from SMAD4 Loss Induces c-MYC–Mediated NLE1 Upregulation to Support Protein Biosynthesis, Colorectal Cancer Growth, and Metastasis
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Supplementary video file from SMAD4 Loss Induces c-MYC–Mediated NLE1 Upregulation to Support Protein Biosynthesis, Colorectal Cancer Growth, and Metastasis
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Supplementary Table S2 from A Tumor-suppressive Molecular Axis EP300/circRERE/miR-6837-3p/MAVS Activates Type I IFN Pathway and Antitumor Immunity to Suppress Colorectal Cancer
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Supplementary Table 2 from N-myc–Mediated Translation Control Is a Therapeutic Vulnerability in Medulloblastoma
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Supplementary Table 3 from N-myc–Mediated Translation Control Is a Therapeutic Vulnerability in Medulloblastoma
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Supplementary Data from SENP1 Decreases RNF168 Phase Separation to Promote DNA Damage Repair and Drug Resistance in Colon Cancer
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Supplementary Table 2 from ESRRB Inhibits the TGFβ Signaling Pathway to Drive Cell Proliferation in Cervical Cancer
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Supplementary Figure S2 from G-CSF Is a Novel Mediator of T-Cell Suppression and an Immunotherapeutic Target for Women with Colon Cancer
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Supplementary Table 2 from ANO1 Reprograms Cholesterol Metabolism and the Tumor Microenvironment to Promote Cancer Metastasis
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Supplementary Table 3 from ANO1 Reprograms Cholesterol Metabolism and the Tumor Microenvironment to Promote Cancer Metastasis
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Supplementary Table 4 from ANO1 Reprograms Cholesterol Metabolism and the Tumor Microenvironment to Promote Cancer Metastasis
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Supplementary Table 6 from ANO1 Reprograms Cholesterol Metabolism and the Tumor Microenvironment to Promote Cancer Metastasis
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Supplementary Table 7 from ANO1 Reprograms Cholesterol Metabolism and the Tumor Microenvironment to Promote Cancer Metastasis
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Supplementary Table 8 from ANO1 Reprograms Cholesterol Metabolism and the Tumor Microenvironment to Promote Cancer Metastasis
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Supplementary Table 9 from ANO1 Reprograms Cholesterol Metabolism and the Tumor Microenvironment to Promote Cancer Metastasis
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Figure 2 from Spatially Resolved Transcriptomics Deconvolutes Prognostic Histological Subgroups in Patients with Colorectal Cancer and Synchronous Liver Metastases
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Figure 3 from Spatially Resolved Transcriptomics Deconvolutes Prognostic Histological Subgroups in Patients with Colorectal Cancer and Synchronous Liver Metastases
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Figure 4 from Spatially Resolved Transcriptomics Deconvolutes Prognostic Histological Subgroups in Patients with Colorectal Cancer and Synchronous Liver Metastases
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Figure 5 from Spatially Resolved Transcriptomics Deconvolutes Prognostic Histological Subgroups in Patients with Colorectal Cancer and Synchronous Liver Metastases
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Figure 6 from Spatially Resolved Transcriptomics Deconvolutes Prognostic Histological Subgroups in Patients with Colorectal Cancer and Synchronous Liver Metastases
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Table 1 from Spatially Resolved Transcriptomics Deconvolutes Prognostic Histological Subgroups in Patients with Colorectal Cancer and Synchronous Liver Metastases
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