Jing Shi , Yebin Yang , Fangci Chen , Linpo Zhou , Haoran Wei , Fanhe Dong , Xiang Wang , Yuqiang Shan , Tianwei Chen
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引用次数: 0
Abstract
Ribosomal protein L36A (RPL36A) was one of the most upregulated proteins in colorectal cancer (CRC), yet its role in colorectal cancer (CRC) remains largely unexplored, with limited studies investigating its expression and biological functions. In this investigation, we confirmed a marked upregulation of RPL36A in CRC tissues, correlating with an adverse prognosis. Silencing RPL36A markedly attenuated CRC cell malignant properties and tumor xenograft growth. Further mechanistic analysis indicated that RPL36A depletion diminished phosphorylated ERK levels, subsequently impacting the expression of c-Myc and ELK1, key downstream effectors in the MAPK/ERK pathway. Notably, the tumor-suppressive effects of RPL36A knockdown could be negated by an ERK activator. Collectively, our findings underscore the oncogenic function of RPL36A in CRC and propose it as a potential target for therapeutic intervention.
期刊介绍：
Translational Oncology publishes the results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of oncology patients. Translational Oncology will publish laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer. Peer reviewed manuscript types include Original Reports, Reviews and Editorials.
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