学科主题临床医学
STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer
Wu, Fan1,2; Gao, Pin1; Wu, Wei1; Wang, Zaozao1; Yang, Jie1; Di, Jiabo1; Jiang, Beihai1; Su, Xiangqian1
通讯作者Jiang, Beihai(1) ; Su, Xiangqian(1)
关键词STK25 GOLPH3 Colorectal cancer (CRC) Glycolysis mTOR
刊名JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
2018-07-11
DOI10.1186/s13046-018-0808-1
37
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]PROTEIN-KINASE STK25 ; UP-REGULATION ; RAPAMYCIN SENSITIVITY ; SIGNALING PATHWAY ; MAMMALIAN TARGET ; SKELETAL-MUSCLE ; GASTRIC-CANCER ; TUMOR-GROWTH ; MTOR ; METABOLISM
英文摘要

Background: Serine/threonine protein kinase 25 (STK25) is critical in regulating whole-body glucose and insulin homeostasis and the accumulation of ectopic lipids. The Warburg effect, also known as aerobic glycolysis, is an essential metabolic characteristic of cancer cells. However, the effects of STK25 on aerobic glycolysis of cancer cells remain unexplored. The aim of this study is to investigate the role of STK25 in colorectal cancer (CRC) and to elucidate the underlying mechanisms.

Methods: The influences of STK25 on the cell proliferation were evaluated by MTT and colony formation assays. The roles of STK25 in aerobic glycolysis were determined by glucose uptake and lactate production assays. The interaction between STK25 and GOLPH3 was detected by co-immunoprecipitation, GST pull-down, and His-tag pull-down assays. Western blot was used to measure the expression of glycolytic genes, and the status of kinases in mTOR pathway. Moreover, a xenograft mouse model was used to investigate the effects of STK25 in vivo. The prognostic significance of STK25 was analyzed using public CRC datasets by a log-rank test.

Results: STK25 suppressed proliferation, glycolysis and glycolytic gene expression in CRC cells. STK25 interacted with GOLPH3 and mediated glycolysis through GOLPH3-regulated mTOR signaling. Consistent with these observations, silencing of STK25 promoted tumor growth and glycolytic gene expression in an in vivo xenograft mouse model. Moreover, high levels of STK25 correlated with favorable prognosis in patients with CRC.

Conclusions: Our results demonstrated that STK25 negatively regulates the proliferation and glycolysis via GOLPH3-dependent mTOR signaling. Accordingly, STK25 could be a potential therapeutic target for the treatment of CRC.

语种英语
WOS记录号WOS:000438205100001
通讯作者邮箱beihai_jiang@bjmu.edu.cn ; suxiangqian@bjmu.edu.cn
第一作者单位Inner Mongolia Peoples Hosp, Hohhot 010010, Peoples R China ; Peking Univ, Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Minist Educ,Dept Gastrointestinal Surg 4, 52 Fucheng Rd, Beijing 100142, Peoples R China
通讯作者单位Peking Univ, Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Minist Educ,Dept Gastrointestinal Surg 4, 52 Fucheng Rd, Beijing 100142, Peoples R China
ISSN1756-9966
引用统计
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/142595
专题北京大学临床肿瘤学院_胃肠肿瘤中心四病区
北京大学第二临床医学院_党委院长办公室
作者单位1.Inner Mongolia Peoples Hosp, Hohhot 010010, Peoples R China;
2.Peking Univ, Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Minist Educ,Dept Gastrointestinal Surg 4, 52 Fucheng Rd, Beijing 100142, Peoples R China
推荐引用方式
GB/T 7714
Wu, Fan,Gao, Pin,Wu, Wei,et al. STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer[J]. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH,2018,37.
APA Wu, Fan.,Gao, Pin.,Wu, Wei.,Wang, Zaozao.,Yang, Jie.,...&Su, Xiangqian.(2018).STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer.JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH,37.
MLA Wu, Fan,et al."STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer".JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH 37(2018).
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