Interaction between C2ORF68 and HuR in human colorectal cancer

Lv, Zhaoxu; He, Kunyan; Shi, Lihong; Shi, Kai; Chen, Yao

doi:10.3892/or.2019.6973

Cited by 3 publications

(5 citation statements)

References 33 publications

(46 reference statements)

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“…HuR is an RNA-binding protein that recognizes U/AU-rich elements in diverse RNAs and post-transcriptionally regulates the fate of target RNAs. HuR regulates cellular responses to differentiation, senescence, inflammatory factors and immune stimuli by tightly controlling the post-transcriptional fate of specific mRNAs (33,34). HuR is expressed at high levels in a number of types of cancers and is believed to promote tumorigenesis by interacting with mRNAs encoding proteins implicated in cell proliferation and survival, angiogenesis, invasion and metastasis (23).…”

Section: Discussionmentioning

confidence: 99%

The role of human antigen R (HuR) in modulating proliferation, senescence and radiosensitivity of skin cells

Feng

Jiang

et al. 2022

Exp Ther Med

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The skin is the largest outermost organ of the human body. It is vulnerable to various damages, such as ionizing radiation. Exploration of proliferation, senescence and radiosensitivity of skin cells contributes to the development of medical and cosmetic countermeasures against skin aging and toward injury protection. Human antigen R (HuR) is one of the most widely studied RNA-binding proteins and serves an important role in stabilization of mRNA and regulation of the expression of the target genes. To investigate the role of HuR in modulating proliferation, senescence and radiosensitivity of skin cells, the present study performed an in vitro study using lentivirus-mediated overexpression or silencing of HuR in human keratinocyte HaCaT cells and human skin fibroblast WS1 cells. The results indicated that overexpression of HuR promoted proliferation, whereas downregulation of HuR inhibited proliferation of HaCaT and WS1 cells. Overexpression of HuR reduced apoptosis and senescence in skin cells. RNA-Seq of skin cells with HuR overexpression or knockdown identified 77 mRNAs positively or negatively correlated with HuR expression levels. In addition, silencing of HuR induced a significant increase in radiogenic reactive oxygen species after irradiation. Overexpression of HuR increased radiotolerance of HaCaT and WS1 cells. RNA immunoprecipitation coupled with RNA-Seq identified 14 mRNAs interacting with HuR upon radiation exposure. Overall, the findings of the present study illustrated the key role of HuR in modulating proliferation, senescence and radiosensitivity of skin cells providing a new therapeutic strategy for cosmetic treatments and to combat skin injury.

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Section: Discussionmentioning

confidence: 99%

The role of human antigen R (HuR) in modulating proliferation, senescence and radiosensitivity of skin cells

Feng

Jiang

et al. 2022

Exp Ther Med

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“…The results from luciferase assay confirmed that miR-519 could directly bind to HUR mRnA and negatively regulate HUR protein expression. HUR is a RNA-binding protein that can bind and stabilize AU rich element-mRNAs (28). HUR is abundantly expressed in cancer cells and associated-malignant phenotypes (29).…”

Section: Discussionmentioning

confidence: 99%

miR‑519 regulates the proliferation of breast cancer cells via targeting human antigen�R

et al. 2019

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Breast cancer is one of the most prevalent types of cancer among women that leads to millions of deaths worldwide every year. The mechanisms of breast cancer pathogenesis remain unclear. It has been reported that aberrant expression of miR-519, is associated with breast cancer development; however, the effects of miR-519 on breast cancer cell proliferation remain unknown. Therefore, the present study aimed to determine whether miR-519 could regulate breast cancer cell proliferation. A total of 20 pairs of primary breast cancer and adjacent normal tissues were collected from patients with breast cancer. miR-519 expression level was determined by reverse transcription-quantitative polymerase chain reaction. Furthermore, miR-519 mimics or inhibitors were transfected into breast cancer MCF-7 cells in order to up-or downregulate miR-519 expression. Subsequently, human antigen R (HUR), BCL-2 and BAX protein levels were analyzed by western blotting. MCF-7 cell proliferation was assessed using MTT and colony formation assays. A luciferase assay was performed to verify whether miR-519 could directly bind to HUR mRNA. The results demonstrated that miR-519 expression level was lower in primary breast cancer tissues compared with adjacent normal tissues. Furthermore, miR-519 overexpression and downregulation inhibited and stimulated MCF-7 cell proliferation, respectively. In addition, the results from luciferase assay demonstrated that HUR was a target of miR-519. HUR overexpression could reverse the effect of miR-519 mimics on MCF-7 cell proliferation, whereas HUR silencing could rescue the effect of miR-519 inhibitors on MCF-7 cell proliferation. These findings suggested that miR-519 may regulate MCF-7 cell proliferation by targeting HUR.

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“…Kang et al, 2008;Lukosiute-Urboniene et al, 2019). In pancreatic ductal adenocarcinoma cells, an inhibitor of apoptosis protein 1 (IAP1) expression is strongly correlated with HuR This molecular event has a synergistic effect on the onset and development of colorectal cancer (Lv et al, 2019). Recent findings have provided evidence for the relationship between HuR and exosomes.…”

Section: Rbps and Rna Stabilitymentioning

confidence: 99%

“…In colorectal cancer cells, HuR interacts with chromosome 2 open reading frame 68 (C2ORF68), which is a potential carcinogenesis‐associated factor. This molecular event has a synergistic effect on the onset and development of colorectal cancer (Lv et al, 2019). Recent findings have provided evidence for the relationship between HuR and exosomes.…”

Section: Function Of Rbps In Cancer Cellsmentioning

confidence: 99%

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The oncogenic and tumor suppressive roles of RNA‐binding proteins in human cancers

Bitaraf

Razmara

Bakhshinejad

et al. 2021

Journal Cellular Physiology

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Posttranscriptional regulation is a mechanism for the cells to control gene regulation at the RNA level. In this process, RNA-binding proteins (RBPs) play central roles and orchestrate the function of RNA molecules in multiple steps. Accumulating evidence has shown that the aberrant regulation of RBPs makes contributions to the initiation and progression of tumorigenesis via numerous mechanisms such as genetic changes, epigenetic alterations, and noncoding RNA-mediated regulations.In this article, we review the effects caused by RBPs and their functional diversity in the malignant transformation of cancer cells that occurs through the involvement of these proteins in various stages of RNA regulation including alternative splicing, stability, polyadenylation, localization, and translation. Besides this, we review the various interactions between RBPs and other crucial posttranscriptional regulators such as microRNAs and long noncoding RNAs in the pathogenesis of cancer. Finally, we discuss the potential approaches for targeting RBPs in human cancers.

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Interaction between C2ORF68 and HuR in human colorectal cancer

Cited by 3 publications

References 33 publications

The role of human antigen R (HuR) in modulating proliferation, senescence and radiosensitivity of skin cells

The role of human antigen R (HuR) in modulating proliferation, senescence and radiosensitivity of skin cells

miR‑519 regulates the proliferation of breast cancer cells via targeting human antigen�R

The oncogenic and tumor suppressive roles of RNA‐binding proteins in human cancers

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