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 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.

Wu X ，Xiao Y ，Yan W ，Ji Z ，Zheng G ... -  《-》

Knockdown of STIL suppresses the progression of gastric cancer by down-regulating the IGF-1/PI3K/AKT pathway.

SCL/TAL1 interrupting locus (STIL) regulates the mitotic centrosome to promote the centriolar replication and cell cycling, and is associated with malignancies. However, the role and mechanism of STIL in gastric cancer (GC) remain elusive. STIL expression in GC tissue microarray was detected by immunohistochemistry (IHC). GC cells were transduced with control lentivirus or lentivirus for expression STIL-specific shRNA and the effect of STIL silencing on the malignant behaviors of GC cells was measured in vitro and in vivo. The potential mechanisms underlying the action of STIL were analyzed by transcriptome microarray and bioinformatics. STIL expression was up-regulated in GC tissues both in our cohort and the data from the cancer genome atlas, and positively associated with T stage and poor overall survival of GC patients. Knockdown of STIL significantly inhibited the proliferation and clonogenicity of human GC cells and attenuated the growth of implanted GC in vivo. Furthermore, STIL silencing induced cell cycle arrest in G2/M phase and apoptosis of GC cells. Transcriptome analysis indicated that STIL silencing modulated many gene expression, particularly for down-regulating the IGF-1/PI3K/AKT pathway. In addition, treatment with SC79, an AKT activator, significantly mitigated the effect of STIL-silencing in GC cells. In conclusion, STIL promotes gastric carcinogenesis and progression by enhancing the IGF-1/PI3K/AKT signaling, and STIL may be a novel target for intervention of GC.

Wang J ，Zhang Y ，Dou Z ，Jiang H ，Wang Y ，Gao X ，Xin X ... -  《-》

Snail promotes cell migration through PI3K/AKT-dependent Rac1 activation as well as PI3K/AKT-independent pathways during prostate cancer progression.

Henderson V ，Smith B ，Burton LJ ，Randle D ，Morris M ，Odero-Marah VA ... -  《-》

PI3K-AKT-mTOR pathway is dominant over androgen receptor signaling in prostate cancer cells.

Kaarbø M ，Mikkelsen OL ，Malerød L ，Qu S ，Lobert VH ，Akgul G ，Halvorsen T ，Maelandsmo GM ，Saatcioglu F ... -  《-》

S100A16 promotes cell proliferation and metastasis via AKT and ERK cell signaling pathways in human prostate cancer.

Zhu W ，Xue Y ，Liang C ，Zhang R ，Zhang Z ，Li H ，Su D ，Liang X ，Zhang Y ，Huang Q ，Liu M ，Li L ，Li D ，Zhao AZ ，Liu Y ... -  《-》