The human oncogene SCL/TAL1 interrupting locus (STIL) promotes tumor growth through MAPK/ERK, PI3K/Akt and AMPK pathways in prostate cancer

The morbidity and mortality of prostate cancer (PCa) in China have increased obviously, which became the second leading cause of death in men with cancer. Hedgehog (Hh) signaling pathway is a key signaling pathway involved in the prostate cancer progression. The human oncogene SCL/TAL1 interrupting...

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Published inGene Vol. 686; pp. 220 - 227
Main Authors Wu, Xingcheng, Xiao, Yu, Yan, Weigang, Ji, Zhigang, Zheng, Guoyang
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 20.02.2019
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Summary:The morbidity and mortality of prostate cancer (PCa) in China have increased obviously, which became the second leading cause of death in men with cancer. Hedgehog (Hh) signaling pathway is a key signaling pathway involved in the prostate cancer progression. The human oncogene SCL/TAL1 interrupting locus (STIL) can modulate the Hh signaling pathway, but its function in PCa has not been reported. Here, we showed that STIL was increased in high grade prostate cancer tissue. Knockdown of STIL in prostate cancer cells PC-3 and DU 145 significantly decreased the proliferation of cells and induced cellular apoptosis through casepase3/7 mediated pathway. Moreover, the colony formation ability was also inhibited when knockdown of STIL by lentivirus-mediated shRNA. Furthermore, the cellular signaling antibody array analysis revealed which signaling pathway was affected when silencing STIL. Altogether, we found that STIL could affect MAPK/ERK, PI3K/Akt and AMPK signaling pathways, thus promoting cellular proliferation, colony formation and suppressing cellular apoptosis in prostate cancer. •The expression of STIL was gradually increased with the grade of prostate cancer.•Knockdown of STIL suppresses the proliferation and induces apoptosis of prostate cancer cells.•STIL silencing regulated tumor growth through MAPK/ERK, PI3K/Akt and AMPK signaling pathways in prostate cancer.
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ISSN:0378-1119
1879-0038
1879-0038
DOI:10.1016/j.gene.2018.11.048