Loss of Insulin-like Growth Factor II Receptor Expression Promotes Growth in Cancer by Increasing Intracellular Signaling from both IGF-I and Insulin Receptors

Insulin-like growth factor 2 and its receptors (IGF 1R and IGF 2R/mannose 6-phosphate) in endometrial adenocarcinoma

“…Furthermore, the IGF2/M6P locus at 6q has been reported to be a hot spot for mutation in tumors, including malignant melanoma [37], ovarian cancer [38] non-Hodgkin lymphoma [39], and renal cell carcinoma [40]. Down regulation of the IGF 2R/M6P promotes the growth of transformed cells by sustaining IGF 2, which binds to and activates IGF 1R and the insulin receptor to increase intracellular growth signals [41]. However, it has also been shown that IGF 2R/M6P is a receptor for granzyme B during immune system mediated apoptosis [42].…”

Germinal tumor invasion and the role of the testicular stroma

“…malignant human tumors. It has been demonstrated that downregulation of IGF-IIR enhances growth in cancer cells by maintaining IGF-II, which activates growth promoting signals through IGF-IR (Osipo et al, 2001). In human lung tumors it has been observed that IGF-I, IGF-II and other growth factors are implicated in the upregulation of MMP-2 and MMP-9 activity and in increased cell migration (Bredin et al, 2003).…”

Clinical significance of loss of heterozygosity for M6P/IGF2R in patients with primary hepatocellular carcinoma

“…Functional studies show the introduction of an exogenous wild-type M6P/IGF2R with a single inactivated allele into human colorectal cancer cells significantly decreases cell growth rate and enhances apoptosis [13] . Conversely, the loss of M6P/IGF2R expression promotes cancer cell growth by increasing intracellular signaling from both the receptors, the insulin-like growth factor 1 receptor and the insulin receptors [22] . Kong et al [10] demonstrated mutations in both alleles of the M6P/IGF2R are found in more than 50% of squamous cell carcinomas of the lung.…”