Impact of RNA‑binding motif 3 expression on the whole transcriptome of prostate cancer cells: An RNA sequencing study

Dong, Qingzhuo; Lv, Chengcheng; Zhang, Gejun; Yu, Zi; Kong, Chuize; Fu, Cheng; Zeng, Yu

doi:10.3892/or.2018.6618

Cited by 3 publications

(3 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As a stress-response protein, RBM3 also has RNA-binding properties which play a crucial role in determining the fate of cancer cells in the tumor microenvironment [ 42 – 44 ]. We have previously shown that the expression of RBM3 was significantly decreased in cells that survived stressful environments, such as high temperature, chemotherapy conditions or a soft agar environment, favoring the enhanced stemness feature of surviving cells by inducing cell quiescence [ 12 , 45 , 46 ]. In the present study, we similarly observed that interaction of PCa cells with the bone microenvironment reduced the expression of RBM3, and this potentially “permitted” the activation of Wnt β -catenin signaling which is critically important for bone metastasis of PCa.…”

Section: Discussionmentioning

confidence: 99%

RBM3 suppresses stemness remodeling of prostate cancer in bone microenvironment by modulating N6-methyladenosine on CTNNB1 mRNA

Zhang

Niu

et al. 2023

Cell Death Dis

View full text Add to dashboard Cite

Bone metastasis is the most happened metastatic event in prostate cancer (PCa) and needs a large effort in treatment. When PCa metastasizes to the bone, the new microenvironment can induce the epigenome reprogramming and stemness remodeling of cancer cells, thereby increasing the adaptability of cancer cells to the bone microenvironment, and this even leads to the occurrence of secondary tumor metastasis. Our group has previously found that RNA binding motif 3 (RBM3) affects the stem cell-like properties of PCa by interfering with alternative splicing of CD44. However, whether RBM3, as a stress-response protein, can resist microenvironmental remodeling of PCa particularly in bone metastasis remains unknown. By co-culturing PCa cells with osteoblasts to mimic PCa bone metastases, we found that RBM3 upregulates the N6-methyladenosine (m6A) methylation on the mRNA of catenin beta 1 (CTNNB1) in a manner dependent on methyltransferase 3 (METTL3), an N6-adenosine-methyltransferase complex catalytic subunit. Consequently, this modification results in a decreased stability of CTNNB1 mRNA and a followed inactivation of Wnt signaling, which ultimately inhibits the stemness remodeling of PCa cells by osteoblasts. Thus, the present study may extend our understanding of the inhibitory role of RBM3 on particularly bone metastasis of PCa.

show abstract

Section: Discussionmentioning

confidence: 99%

RBM3 suppresses stemness remodeling of prostate cancer in bone microenvironment by modulating N6-methyladenosine on CTNNB1 mRNA

Zhang

Niu

et al. 2023

Cell Death Dis

View full text Add to dashboard Cite

show abstract

“…Recent evidence has shown that H3 acetylation of the transcription intermediary factor (TIF) family of proteins is important for cell proliferation in a number of different cancers (26)(27)(28)(29). We hypothesized that KAT2B enhanced H3K14 acetylation of TIF proteins, which then acted as transcriptional activators enhancing downstream gene expression, resulting in improved YAP stability and promoting NPC proliferation.…”

Section: Binding Of Tif1a To H3k14ac Is Required For Afap1-as1-drivenmentioning

confidence: 99%

Long Noncoding RNA AFAP1-AS1 Is a Critical Regulator of Nasopharyngeal Carcinoma Tumorigenicity

et al. 2020

View full text Add to dashboard Cite

BackgroundThe long noncoding RNA actin filament associated protein 1 antisense RNA1 (AFAP1-AS1) is a critical player in various cancers. However, the clinical value and functional mechanisms of AFAP1-AS1 during the tumorigenicity of nasopharyngeal carcinoma (NPC) remain unclear. Here, we investigated the clinical application and potential molecular mechanisms of AFAP1-AS1 in NPC tumorigenesis and progression.MethodsThe expression level of AFAP1-AS1 was determined by qRT-PCR in 10 paired fresh human NPC tissues and adjacent normal tissues. RNAscope was performed on 100 paired paraffin-embedded NPC and adjacent nontumor specimens. The biological functions of AFAP1-AS1 were assessed by in vitro and in vivo functional experiments. RNA-protein pull-down assays were performed to detect and identify the AFAP1-AS1-interacting protein KAT2B. Protein-RNA immunoprecipitation (RIP) assays were conducted to examine the interaction of AFAP1-AS1 and KAT2B. Chromatin immunoprecipitation (ChIP) and luciferase analyses were utilized to identify the binding site of transcription intermediary factor 1 alpha (TIF1α) and H3K14ac on the RBM3 promoter.ResultsAFAP1-AS1 is upregulated in NPC and is a poor prognostic indicator for survival in NPC patients. AFAP1-AS1 was required for NPC proliferation in vitro and tumorigenicity in vivo. Mechanistic investigations suggested that AFAP1-AS1 binds to KAT2B and promotes acetyltransferase activation at two residues (E570/D610). KAT2B further promotes H3K14 acetylation and protein binding to the bromo domain of TIF1α. Consequently, TIF1α acts as a nuclear transcriptional coactivator of RBM3 transcription, leading to YAP mRNA stabilization and enhanced NPC tumorigenicity.ConclusionsOur findings suggest that AFAP1-AS1 functions as an oncogenic biomarker and promotes NPC tumorigenicity through enhanced KAT2B acetyltransferase activation and YAP mRNA stabilization.

show abstract

“…RBM3 inhibits CD44v8‐v10 splicing to attenuate the stem cell‐like character of prostate cancer cells (Dong et al, 2018; Zeng et al, 2013). Meanwhile, RBM3 inhibits glycogen synthase kinase‐3β, activity and stimulates the Wnt/β‐catenin pathway, thereby enhancing the stem cell characteristics of colorectal cancer cells (Venugopal et al, 2016).…”

Section: Rbm3 and Its Multiple Functionsmentioning

confidence: 99%

RBM3 is an outstanding cold shock protein with multiple physiological functions beyond hypothermia

Quan

Fan

et al. 2022

Journal Cellular Physiology

View full text Add to dashboard Cite

RNA‐binding motif protein 3 (RBM3), an outstanding cold shock protein, is rapidly upregulated to ensure homeostasis and survival in a cold environment, which is an important physiological mechanism in response to cold stress. Meanwhile, RBM3 has multiple physiological functions and participates in the regulation of various cellular physiological processes, such as antiapoptosis, circadian rhythm, cell cycle, reproduction, and tumogenesis. The structure, conservation, and tissue distribution of RBM3 in human are demonstrated in this review. Herein, the multiple physiological functions of RBM3 were summarized based on recent research advances. Meanwhile, the cytoprotective mechanism of RBM3 during stress under various adverse conditions and its regulation of transcription were discussed. In addition, the neuroprotection of RBM3 and its oncogenic role and controversy in various cancers were investigated in our review.

show abstract

Impact of RNA‑binding motif 3 expression on the whole transcriptome of prostate cancer cells: An RNA sequencing study

Cited by 3 publications

References 29 publications

RBM3 suppresses stemness remodeling of prostate cancer in bone microenvironment by modulating N6-methyladenosine on CTNNB1 mRNA

RBM3 suppresses stemness remodeling of prostate cancer in bone microenvironment by modulating N6-methyladenosine on CTNNB1 mRNA

Long Noncoding RNA AFAP1-AS1 Is a Critical Regulator of Nasopharyngeal Carcinoma Tumorigenicity

RBM3 is an outstanding cold shock protein with multiple physiological functions beyond hypothermia

Contact Info

Product

Resources

About