Silencing HMGN5 suppresses cell growth and promotes chemosensitivity in esophageal squamous cell carcinoma

被引:10
作者
Liu, Xiaoping [1 ]
Ma, Weiping [1 ]
Yan, Yanli [1 ]
Wu, Suge [1 ]
机构
[1] Xi An Jiao Tong Univ, Ctr Canc, Affiliated Hosp 1, Xian 710061, Shaanxi, Peoples R China
关键词
chemosensitivity; cisplatin; esophageal squamous cell carcinoma; HMGN5; BINDING DOMAIN 5; PROSTATE-CANCER CELLS; IN-VITRO; TARGETING HMGN5; BLADDER-CANCER; BREAST-CANCER; INVASION; PROLIFERATION; EXPRESSION; METASTASIS;
D O I
10.1002/jbt.21996
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Previous study has demonstrated that high mobility group nucleosome-binding domain 5 (HMGN5) is involved in tumorigenesis and the development of multidrug resistance in several human cancers. However, the role of HMGN5 in esophageal squamous cell carcinoma (ESCC) remains unclear. Here, we showed that HMGN5 was significantly upregulated in ESCC cells. Knockdown of HMGN5 significantly inhibited cell growth and induced cell apoptosis of ESCC cells. Moreover, knockdown of HMGN5 increased the sensitivity of ESCC cells towards cisplatin. By contrast, overexpression of HMGN5 showed the opposite effects. Further experiments demonstrated that HMGN5 regulated the expression of multidrug resistance 1, cyclin B1, and Bcl-2. Overall, our results reveal that HMGN5 promotes tumor progression of ESCC and is also an important regulator of chemoresistance. Our study suggests that inhibition of HMGN5 may be a potential strategy for improving effectiveness of ESCC treatment.
引用
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页数:8
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共 32 条
[31]   Small interfering RNA targeting HMGN5 induces apoptosis via modulation of a mitochondrial pathway and Bcl-2 family proteins in prostate cancer cells [J].
Zhang, Xiao-Yu ;
Guo, Zhong-Qiang ;
Ji, Shi-Qi ;
Zhang, Min ;
Jiang, Ning ;
Li, Xue-Song ;
Zhou, Li-Qun .
ASIAN JOURNAL OF ANDROLOGY, 2012, 14 (03) :487-492
[32]   The expression and clinical significance of high mobility group nucleosome binding domain 5 in human osteosarcoma [J].
Zhou, Xuhui ;
Yuan, Bo ;
Yuan, Wen ;
Wang, Ce ;
Gao, Rui ;
Wang, Junyan .
TUMOR BIOLOGY, 2014, 35 (07) :6539-6547