TH1L involvement in colorectal cancer pathogenesis by regulation of CCL20 through the NF-κB signalling pathway

被引:0
作者
Wang, Shaochang [1 ]
Sun, Yujing [2 ]
Li, Chunya [1 ]
Chong, Yueyang [1 ,3 ]
Ai, Meihong [1 ]
Wang, Yanxia [1 ]
Shi, Haiyun [4 ]
Shang, Yu [1 ]
机构
[1] Beijing Normal Univ, Coll Life Sci, Key Lab Cell Proliferat & Regulat Biol, Minist Educ, Beijing 100875, Peoples R China
[2] Peking Univ, Dept Lab Med, Int Hosp, Beijing, Peoples R China
[3] Xi An Jiao Tong Univ, Affiliated Hosp 1, Med X Inst, Dept Canc Precis Med, Xian, Peoples R China
[4] Capital Med Univ, Beijing Key Lab Precancerous Les Digest Dis, Beijing Digest Dis Ctr, Dept Gastroenterol,Beijing Friendship Hosp,Natl Cl, Beijing, 100050, Peoples R China
基金
中国国家自然科学基金;
关键词
CCL20; colorectal cancer (CRC); NF-kappa B signalling pathway; TH1L; TRIHYDROPHOBIN; 1; CHROMOSOME; 20Q; STOOL DNA; INFLAMMATION; STATISTICS; EXPRESSION; ADENOMA; CELLS; GENE;
D O I
暂无
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
TH1L (also known as NELF-C/D) is a member of the Negative Elongation Factor (NELF) complex, which is a metazoan-specific factor that regulates RNA Polymerase II (RNAPII) pausing and transcription elongation. However, the function and molecular mechanisms of TH1L in cancer progression are still largely unknown. In this study, we found that TH1L was highly expressed in colorectal cancer (CRC) tissues and the faeces of CRC patients. Overexpression of TH1L significantly enhanced the proliferation and migration of CRC cells, while its knockdown markedly suppressed these processes. In mechanism, RNA sequencing revealed that CCL20 was upregulated in TH1L-overexpressed CRC cells, leading to activation of the NF-kappa B signalling pathway. Rescue assays showed that knockdown of CCL20 could impair the tumour-promoting effects of THIL in CRC cells. Taken together, these results suggest that TH1L may play a vital role via the CCL20/NF-kappa B signalling pathway in CRC proliferation and migration and may serve as a potential target for diagnosis and therapy of CRC.
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页数:12
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