Long noncoding RNA ARSR is associated with a poor prognosis in patients with colorectal cancer
Autor: | Houbo Deng, Xuezhu Jin, Jingrong Dong, Ting Li |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Male Colorectal cancer Carcinogenesis Drug resistance medicine.disease_cause 03 medical and health sciences 0302 clinical medicine Drug Discovery Genetics Medicine Gene silencing Humans Viability assay Molecular Biology Genetics (clinical) Aged business.industry Middle Aged medicine.disease Prognosis digestive system diseases Long non-coding RNA Oxaliplatin Gene Expression Regulation Neoplastic 030104 developmental biology Apoptosis Drug Resistance Neoplasm 030220 oncology & carcinogenesis Cancer research Molecular Medicine Female RNA Long Noncoding business Colorectal Neoplasms medicine.drug |
Zdroj: | The journal of gene medicineREFERENCES. 22(10) |
ISSN: | 1521-2254 |
Popis: | Background As one of the leading cancer-related mortalities worldwide, colorectal cancer (CRC) shows resistance to chemotherapy mainly because of drug resistance. Existing evidence has revealed that long noncoding RNAs (lncRNAs) are related to tumorigenesis and chemoresistance scenarios. However, the mechanism by which lncRNA induces chemoresistance and the postoperative prognosis of CRC both remain unclear. Methods The expression of a lncRNA named lncARSR in CRC tissue was tested, and its association with clinical and pathological features was analyzed. Gain-of-function and loss-of-function assays were conducted to investigate the role of lncARSR in vivo and in vitro. Results Functional analysis showed that overexpressing lncARSR increased oxaliplatin (OXA) resistance of CRC cells in vitro and in vivo. Moreover, lncARSR conferred chemoresistance to CRC cells. Silencing lncARSR decreased cell viability and promoted cell apoptosis after OXA treatment, whereas overexpression of lncARSR increased cell viability and reduced cell apoptosis after OXA treatment. In addition, lncARSR overexpression induced the tumor formation capacity of colorectal cancer cells. Conclusions The results obtained in the present study show that up-regulation of lncARSR promoted OXA resistance in CRC. Our results also imply that lncARSR may be a candidate marker for CRC chemoresistance. |
Databáze: | OpenAIRE |
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