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pmid:34680556

A New Light on Potential Therapeutic Targets for Colorectal Cancer Treatment.

Wei-Lun Tsai · Chih-Yang Wang · Yu-Cheng Lee · Wan-Chun Tang · Gangga Anuraga · Hoang Dang Khoa Ta · Yung-Fu Wu · Kuen-Haur Lee

Biomedicines · 2021 doi:10.3390/biomedicines9101438

Paper

complete

Experiment

partial

Data

partial

Analysis

partial

Execution

absent

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A New Light on Potential Therapeutic Targets for Colorectal Cancer Treatment.
doi
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pmid
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Wei-Lun Tsai
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Chih-Yang Wang
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Yu-Cheng Lee
[3]
Wan-Chun Tang
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Gangga Anuraga
[5]
Hoang Dang Khoa Ta
[6]
Yung-Fu Wu
[7]
Kuen-Haur Lee
journal
Biomedicines
year
2021
abstract
The development and progression of colorectal cancer (CRC) involve changes in genetic and epigenetic levels of oncogenes and/or tumor suppressors. In spite of advances in understanding of the molecular mechanisms involved in CRC, the overall survival rate of CRC still remains relatively low. Thus, more research is needed to discover and investigate effective biomarkers and targets for diagnosing and treating CRC. The roles of long non-coding RNAs (lncRNAs) participating in various aspects of cell biology have been investigated and potentially contribute to tumor development. Our recent study also showed that CRNDE was among the top 20 upregulated genes in CRC clinical tissues compared to normal colorectal tissues by analyzing a Gene Expression Omnibus (GEO) dataset (GSE21815). Although CRNDE is widely reported to be associated with different types of cancer, most studies of CRNDE were limited to examining regulation of its transcription levels, and in-depth mechanistic research is lacking. In the present study, CRNDE was found to be significantly upregulated in CRC patients at an advanced TNM stage, and its high expression was correlated with poor outcomes of CRC patients. In addition, we found that knocking down CRNDE could reduce lipid accumulation through the miR-29b-3p/ANGPTL4 axis and consequently induce autophagy of CRC cells.
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In addition, we found that knocking down CRNDE could reduce lipid accumulation through the miR-29b-3p/ANGPTL4 axis and consequently induce autophagy of CRC cells.
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In addition, we found that knocking down CRNDE could reduce lipid accumulation through the miR-29b-3p/ANGPTL4 axis and consequently induce autophagy of CRC cells.
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