Overexpression of long non-coding RNA urothelial carcinoma associated 1 causes paclitaxel (Taxol) resistance in colorectal cancer cells by promoting glycolysis

被引：14
作者：
Shi, Huijuan [1 ]
Li, Kejun [2 ]
Feng, Jinxin [2 ]
Zhang, Xiangliang [2 ]
机构：
[1] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Pathol, Guangzhou, Guangdong, Peoples R China
[2] Guangzhou Med Univ, Dept Abdominal Surg, Affiliated Canc Hosp & Inst, Guangzhou, Guangdong, Peoples R China
来源：
JOURNAL OF CHEMOTHERAPY | 2021年 / 33卷 / 06期
关键词：
Colorectal cancer; lncRNA UCA1; paclitaxel resistance; glycolysis; HK2; LDHA; AEROBIC GLYCOLYSIS; DRUG-RESISTANCE; UCA1; LNCRNA;
D O I：
10.1080/1120009X.2021.1906032
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Some colorectal cancer patients show resistance to conventional chemotherapeutic agents including Taxol. This study investigated the roles of lncRNA urothelial carcinoma-associated 1 (UCA1) in the modulation of Taxol resistance in human colorectal cancer cells. According to our results, UCA1 was significantly upregulated in colon cancer cell lines/tissues. Construction of the UCA1 overexpression vector revealed that high UCA1 expression was responsible for Taxol resistance and that Taxol can induce UCA1 expression. Importantly, Taxol-resistant cells had a higher glycolysis rate and upregulated expression of the key glycolysis enzymes hexokinase 2 (HK2) and lactate dehydrogenase A (LDHA) than Taxol-sensitive cells. Further research demonstrated that UCA1 could directly regulate glycolysis by regulating HK2 and LDHA expression, which contributes to Taxol resistance. UCA1 is a potential target to overcome chemoresistance in colorectal cancer. We report the modulation of UCA-1-regulated glycolysis as a novel anticancer strategy along with the novel role of UCA1 in Taxol resistance.
引用
收藏
页码：409 / 419
页数：11
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