RNA-binding protein RBM6 as a tumor suppressor gene represses the growth and progression in laryngocarcinoma

Wang, Qiwei; Wang, Fang; Zhong, Waisheng; Ling, Hang; Wang, Jixuan; Cui, Jie; Xie, Tao; Wen, Senli; Chen, Jie

doi:10.1016/j.gene.2019.02.025

Cited by 25 publications

(21 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It belongs to a large RNA binding protein family that plays an essential role in almost every aspect of RNA metabolism, including RNA splicing, and stability 29,30 . A few studies have implicated that RBM6 functions as a tumor suppressor and controls tumor growth by regulating RNA alternative splicing in tumors 31,32 ; however, its function remains largely unexplored. Analysis of RNA-seq data revealed that MLKL inhibition by NSA suppressed the expression of numerous inflammatory-related genes ( Fig.…”

Section: Mlkl Interacts With Rbm6 In Regulating the Mrna Stability Ofmentioning

confidence: 99%

A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression

et al. 2020

View full text Add to dashboard Cite

Mixed-lineage kinase domain-like protein (MLKL) is known as the terminal executor of necroptosis. However, its function outside of necroptosis is still not clear. Herein, we demonstrate that MLKL promotes vascular inflammation by regulating the expression of adhesion molecules ICAM1, VCAM1, and E-selectin in endothelial cells (EC). MLKL deficiency suppresses the expression of these adhesion molecules, thereby reducing EC-leukocyte interaction in vitro and in vivo. Mechanistically, we show that MLKL interacts with RBM6 to promote the mRNA stability of adhesion molecules. In conclusion, this study identified a novel role of MLKL in regulating endothelial adhesion molecule expression and local EC-leukocyte interaction during acute inflammation.

show abstract

Section: Mlkl Interacts With Rbm6 In Regulating the Mrna Stability Ofmentioning

confidence: 99%

A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression

et al. 2020

View full text Add to dashboard Cite

show abstract

“…EGFR is a receptor that promotes tumor occurrence and development; its expression in tumor tissues is higher than that in adjacent and normal tissues. High expression of RBM6 decreased the expression of the protein levels of EGFR, ERK, and p-ERK in vivo and in vitro (63). All these results indicate that RBM6 is a tumor suppressor; however, research on RBM6 is still very limited, and more is needed in the future to fully characterize RBM6 function in disease systems.…”

Section: Rna-binding Motif Protein 10 and Rna-binding Motif Protein 10 Tumor Inhibitory Effectsmentioning

confidence: 95%

RBM10 Regulates Tumor Apoptosis, Proliferation, and Metastasis

Cao

Zhang

et al. 2021

Front. Oncol.

View full text Add to dashboard Cite

The RNA-binding motif protein 10 (RBM10) is involved in alternative splicing and modifies mRNA post-transcriptionally. RBM10 is abnormally expressed in the lung, breast, and colorectal cancer, female genital tumors, osteosarcoma, and other malignant tumors. It can inhibit proliferation, promote apoptosis, and inhibit invasion and metastasis. RBM10 has long been considered a tumor suppressor because it promotes apoptosis through the regulation of the MDM2-p53 negative feedback loop, Bcl-2, Bax, and other apoptotic proteins and inhibits proliferation through the Notch signaling and rap1a/Akt/CREB pathways. However, it has been recently demonstrated that RBM10 can also promote cancer. Given these different views, it is necessary to summarize the research progress of RBM10 in various fields to reasonably analyze the underlying molecular mechanisms, and provide new ideas and directions for the clinical research of RBM10 in various cancer types. In this review, we provide a new perspective on the reasons for these opposing effects on cancer biology, molecular mechanisms, research progress, and clinical value of RBM10.

show abstract

“…This gene has been shown to be deleted or disrupted in lung cancers [122]. Furthermore, RBM6 was reported to inhibit invasion and induce apoptosis, consequently suppressing the cancer cell growth and progression in laryngocarcinoma [123]. Together, these lines of evidence suggest that both RBM5 and RBM6 might play a tumor suppressive role in different types of cancers.…”

Section: Tumor Suppressive Functions Of Rbm10 In Cancer Cellsmentioning

confidence: 95%

RBM10, a New Regulator of p53

Jung

Lee

Zeng

et al. 2020

Cells

View full text Add to dashboard Cite

The tumor suppressor p53 acts as a transcription factor that regulates the expression of a number of genes responsible for DNA repair, cell cycle arrest, metabolism, cell migration, angiogenesis, ferroptosis, senescence, and apoptosis. It is the most commonly silenced or mutated gene in cancer, as approximately 50% of all types of human cancers harbor TP53 mutations. Activation of p53 is detrimental to normal cells, thus it is tightly regulated via multiple mechanisms. One of the recently identified regulators of p53 is RNA-binding motif protein 10 (RBM10). RBM10 is an RNA-binding protein frequently deleted or mutated in cancer cells. Its loss of function results in various deformities, such as cleft palate and malformation of the heart, and diseases such as lung adenocarcinoma. In addition, RBM10 mutations are frequently observed in lung adenocarcinomas, colorectal carcinomas, and pancreatic ductal adenocarcinomas. RBM10 plays a regulatory role in alternative splicing. Several recent studies not only linked this splicing regulation of RBM10 to cancer development, but also bridged RBM10′s anticancer function to the p53 pathway. This review will focus on the current progress in our understanding of RBM10 regulation of p53, and its role in p53-dependent cancer prevention.

show abstract

RNA-binding protein RBM6 as a tumor suppressor gene represses the growth and progression in laryngocarcinoma

Cited by 25 publications

References 30 publications

A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression

A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression

RBM10 Regulates Tumor Apoptosis, Proliferation, and Metastasis

RBM10, a New Regulator of p53

Contact Info

Product

Resources

About