RBM47 Inhibits Hepatocellular Carcinoma Progression as a DNA/RNA Regulator
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ABSTRACT:
PROVIDER: PRJNA833425 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:After ChIP assay, DNA sequencing was conducted to analyze the specific loci binding by RBM47 in HCCLM3 cells.
2025-04-28 | GSE201818 | GEO
Project description:By RIP sequencing, we determined that RBM47 modulated UPF1 by stabilizing its mRNA and addressed the novel motif in the UPF1 3’UTR with direct binding.
2025-04-28 | GSE201892 | GEO
Project description:Hepatocellular carcinoma (HCC) continues to claim a significant number of lives worldwide, yet the molecular drivers behind its progression remain elusive. Despite the annotation of thousands of long non-coding RNAs (lncRNAs) as transcriptional products, their specific roles in suppressing HCC remain poorly understood. Here, we have uncovered LINC00862, a lncRNA that exhibits pronounced downregulation in HCC tissues and whose expression levels linked positively to favorable HCC outcomes, as a function of tumor stage and size. Through in-depth functional assays, we have established the formidable anti-tumor effects of LINC00862 on HCC processes such as proliferation, invasion, metastasis, and growth in both in vitro and in vivo settings. Mechanistically, our detailed RNA sequencing and quantitative proteomics analyses revealed that LINC00862's downstream target effector in HCC cells is RBM47. Our further experimentation strongly supports RBM47 as a central mediator of LINC00862's profound tumor-suppressive effects. Furthermore, we discovered the critical role of Hoogsteen pairing in LINC00862's ability to bind to the RBM47 promoter and recruit CHD5 as a transcription factor, promoting RBM47 transcriptional upregulation in HCC cells. It is intriguing to note that we also discovered that RBM47 is able to act as a transcription factor, positively regulating LINC00862 expression. Our identification of a positive feedback loop involving LINC00862 and RBM47 expands our comprehension of the intricate regulatory network that shapes HCC pathogenesis. LINC00862 represents a promising molecular marker for HCC diagnosis and therapeutics.
2026-01-12 | GSE234454 | GEO
Project description:LINC00862 Inhibits Hepatocellular Carcinoma via a RBM47-mediated Positive Feedback Loop
| PRJNA981470 | ENA
Project description:Through integrative analysis of clinical breast cancer gene expression datasets, cell line models of breast cancer progression, and mutation data from cancer genome resequencing studies, we have identified RNA binding motif protein 47 (RBM47) as a candidate suppressor of breast cancer metastasis. RBM47 inhibited breast cancer progression in experimental models. Transcriptome-wide analysis of RBM47 localization by HITS-CLIP revealed widespread binding to mRNAs, preferentially at the 3' UTRs. RBM47 altered the abundance of a subset of its target mRNAs. Some of the mRNAs stabilized by RBM47, as exemplified by dickkopf WNT signaling pathway inhibitor 1 (DKK1), mediate tumor suppressive effects downstream of RBM47. This work identifies RBM47 as a suppressor of breast cancer progression and highlights the potential of global RNA modulatory events as a source of metastasis-promoting phenotypic traits. Cancer cells transduced with doxycycline-inducible wildtype RBM47 or the RBM47-I281fs mutant, treated with increasing concentrations of doxycycline.
2014-06-11 | E-GEOD-53779 | biostudies-arrayexpress
Project description:Through integrative analysis of clinical breast cancer gene expression datasets, cell line models of breast cancer progression, and mutation data from cancer genome resequencing studies, we have identified RNA binding motif protein 47 (RBM47) as a candidate suppressor of breast cancer metastasis. RBM47 inhibited breast cancer progression in experimental models. Transcriptome-wide analysis of RBM47 localization by HITS-CLIP revealed widespread binding to mRNAs, preferentially at the 3' UTRs. RBM47 altered the abundance of a subset of its target mRNAs. Some of the mRNAs stabilized by RBM47, as exemplified by dickkopf WNT signaling pathway inhibitor 1 (DKK1), mediate tumor suppressive effects downstream of RBM47. This work identifies RBM47 as a suppressor of breast cancer progression and highlights the potential of global RNA modulatory events as a source of metastasis-promoting phenotypic traits.
2014-06-11 | GSE53779 | GEO
Project description:The mechanisms by which the tumor behaviors of hepatocellular carcinoma (HCC) support growth and metastasis remain largely unknown, and it has become increasingly apparent that molecular dysregulation is of considerable importance for cellular signaling pathways. Recently, RNA-binding motif protein 47 (RBM47) has been suggested to function as a tumor regulator by acting as an RNA binding protein (RBP), but its role in HCC remains ambiguous. Here, in HCC, we identified that RBM47 had an inhibitory influence on tumor behaviors in vitro and accordingly suppressed the growth and metastasis of xenograft tumors in vivo. Additionally, RBM47 was verified to positively regulate Upframeshift 1 (UPF1), which is a crucial protein involved in the nonsense-mediated RNA decay (NMD) process and was previously determined to be an HCC suppressor. Mechanistically, the stability of UPF1 mRNA was demonstrated to be enhanced with its 3'UTR bound by RBM47, which acted as an RNA binding protein. Meanwhile, RBM47 was also proven to promote the transcription of UPF1 as a transcription factor. Taken together, we concluded that RBM47 functioned as a tumor suppressor by upregulating UPF1, acting as a DNA/RNA binding protein at the transcriptional and posttranscriptional levels.
| S-EPMC9279423 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-04-28 | GSE201893 | GEO