2013
DOI: 10.1016/j.gene.2012.09.080
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Insulin-like factor binding protein-3 promotes the G1 cell cycle arrest in several cancer cell lines

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Cited by 20 publications
(16 citation statements)
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“…IGFBP-3 induces G1 cell cycle arrest and apoptosis in several cancer cell lines, including human NSCLC [44]. The alteration of this protein by oncogenic Akt can be considered as a new cancer therapeutic target.…”
Section: New Advances In Metabolism and Cancer---glycolytic Factormentioning
confidence: 99%
“…IGFBP-3 induces G1 cell cycle arrest and apoptosis in several cancer cell lines, including human NSCLC [44]. The alteration of this protein by oncogenic Akt can be considered as a new cancer therapeutic target.…”
Section: New Advances In Metabolism and Cancer---glycolytic Factormentioning
confidence: 99%
“…So, the aberrant increase of NNMT in GSCs may also be associated with GSCs development. In addition, the insulin-like factor binding protein-3 (IGFBP3), which was found noticeably increased in GSCs, has been reported to be a multi-functional protein that is known to induce apoptosis of various cancer cells by the activation of caspases and the induction of cell cycle arrest [Wu et al, 2013]. In this study, such factor as sex should not be considered because both human GSCs and human NSCs were derived from male patients, so, the deletion or decrease of Sox1 in GSCs may contribute to the malignant transition of NSCs to GSCs.…”
Section: Discussionmentioning
confidence: 99%
“…Activation of MYC was previously identified as a signature of cancer proliferation (42) and a key regulatory feature of basal-like cancers (5). Several of the p53 and MYC-regulated phosphoproteins with sites specific for basal tumor type were also linked to the EGF/EGFR (ErbB-1) and TGFÎČ1 signaling pathways, including phosphoproteins IBP3 (43), FSTL3 (44), and STC2 (41, 45), all of which were subsequently found to have basal-specific phosphosites qualified in plasma. Several phosphoproteins with luminal-specific phosphosites were also identified, and involved the AKT and estrogen mediated signaling pathways, including a HIFα1-regulated oncogene HER2 (ErbB2).…”
Section: Discussionmentioning
confidence: 99%