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Entity | Cancer, across types |
Note | The diversity of biological ligands underlies the role of LRs in multiple pathologic processes, that include atherosclerosis (Tanaga et al., 2004; Seki et al., 2005) Alzheimer's disease (Jaeger and Pietrzik, 2008; Lillis et al., 2008; Wagner and Pietrzik, 2012) and cancer, the focus of this description below. LRP1B, a member of the low-density lipoprotein (LDL) receptor family, was identified as a putative tumor suppressor. The down-expression of LRP1B was observed in multiple primary cancers. |
Oncogenesis | The "signature" of LRP1B inactivation is archetypal of a tumor suppressor gene and reflects selection towards bi-allelic inactivation and complete abrogation of the gene function. In tumors, one can observe that multiple inactivation hits, of structural and regulatory nature, have taken place, on both alleles through diverse combinations of events such as genetic deletions (observable by homozygous deletion), accompanied by epigenetic silencing (DNA methylation), or sometimes by microRNA overexpression (Prazeres et al., 2011). The role of LRP1B as a tumor suppressor may result from modulation of cell migration and invasive capacity, through regulation of the urokinase plasminogen system (Liu et al., 2001). Cells expressing LRP1B display a substantially slower rate of uPA/PAI-1 complex internalization (Knisely et al., 2007) which impairs the regeneration of unoccupied uPAR on the cell surface and correlates with a diminished rate of cell migration (Li et al., 2002; Tanaga et al., 2004). Aside from members of the plasminogen system, LRP1B expression has been shown to deplete the extracellular medium of MMP2 and other factors (Prazeres et al., 2011). These results support the hypothesis that LRP1B endocytosis may (directly or indirectly) constrain the abundance of critical factors in the tumor microenvironment. |
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Entity | Lung cancer |
Note | Nagayama, Kohno et al. (2007) have described that homozygous deletions (HD) was searched for in 43 lung cancer cell lines. The gene LRP1B was also included among the genes. Fifty-one homozygous deletions regions containing 113 genes were identified. The LRP1B was the third most frequent targets of HD. All eight HD segments at the LRP1B gene locus detected in that study included its coding exons, consistent with previous reports (Liu et al., 2000a; Sonoda et al., 2004). At present, the pathogenic significance of LRP1B deletions is unclear; however, frequent HD in these loci indicates that the inactivation of this gene has major roles in the development of lung cancer. LRP1B was mapped at the fragile sites, FRA2F, FRA3B, and FRA16D, and had been found homozygously deleted in a subset of lung cancers (Liu et al., 2000a; Zöchbauer-Müller et al., 2000; Paige et al., 2001; Fabbri et al., 2005; Smith et al., 2006). Kohno, Otsuka et al. (2010) have verified homozygous deletions in 176 genes. They consisted of 171 protein-encoding genes and five miRNA genes. These 176 genes were located in 45 regions on 17 chromosomes. They included known tumor suppressor genes, as well as candidate tumor suppressor genes shown to be hemizygously or homozygously deleted in several types of human cancers, such as LRP1B (Sonoda et al., 2004). |
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Entity | Esophageal carcinoma |
Note | The expression of LRP1B mRNA is frequently lost in esophageal squamous cell carcinoma (ESCs) as a consequence of either homozygous deletions or DNA methylation and the re-expression of this gene inhibits growth of ESC cells. These two types of events affecting the LRP1B gene may be useful as novel diagnostic markers for ESC because of their high frequencies, although it remains unclear whether precancerous lesions of this tumor contain either of those alterations. The apparent multiplicity of tumor-suppressing activities of LRP1B, however, suggests that this molecule might be a useful starting point for development of novel therapeutic strategies (Sonoda et al., 2004). |
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Entity | Oral carcinoma |
Note | Genome-wide LOH analysis demonstrated high LOH ratio of 2q21-23 region by using the markers D2S1334 and D2S1399 in head and neck cancer (Beder et al., 2003). So far no other study showed frequent LOH of this region in oral cancer, but it has been suggested that at least one tumor suppressor gene exists at 2q21-24 and involves in the carcinogenesis of various cancers including oral carcinoma. One candidate gene could be LRP1B, which has already been proposed to function as a tumor suppressor (Cengiz et al., 2007). |
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Entity | Breast cancer |
Note | Kadota, Yang et al. (2010) have observed intragenic deletions within several genes which potentially function as breast cancer tumor suppressor loci. These included deletions which disrupted LRP1B in MCF10CA1h and MCF10CA1a cell lines. |
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Entity | Renal cancer |
Prognosis | In urothelial cancer, only 8% of cases with Grade 1 and none with Grade 2 tumors showed loss of heterozygosity at the LRP1B gene, whereas 49% of the Grade 3 cases had allelic loss at the LRP1B genomic region, which can be taken to indicate that alteration of the LRP1B gene region is associated with high grade of urothelial cancer (Langbein et al., 2002). |
Oncogenesis | Ni, Hu et al. (2013) have investigated the expression of LRP1B in Renal cell cancer (RCC) and its function on cell migration. They found that LRP1B mRNA was widely expressed in the normal renal tubular epithelial cells, but it was frequently down-expressed in RCC tissues and cell lines. The depletion of LRP1B increased the anchorage-independent growth, cell migration and invasion in vitro. Moreover, the expression and activation of Rho family members, actin cytoskeletons and focal adhesions complex (FAC) were also affected, indicating that down-expression of LRP1B led to the increase of cell migration and invasion, which is possibly mediated by actin cytoskeleton remodeling, and expressional alteration of FAC components. At the same time, they also found that silencing of LRP1B obviously occurred in T1 of TNM. The result suggests that silencing of LRP1B is an early event in RCC. Their observation provided an insight into the potential contribution of LRP1B to tumorigenesis, and that LRP1B may be explored as a molecular target in RCC therapy by regulated epigenetic activation means. These functional specificities in cell spreading, migration and invasion strongly validated that LRP1B may function as a tumor suppressor, and exert opposite effects to LRP1 on cell transformation and malignant progression. |
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Entity | Glioma |
Note | Data analysis of full-coverage chromosome 19 highlighted two main regions of copynumber gain, never described before in gliomas, at 19p13.11 and 19q13.13-13.2. Genomic hotspot detection facilitated the identification of small intervals resulting in positional candidate genes such as LRP1B (2q22.3) for losses, and other for gains. These data increase the current knowledge about cryptic genetic changes in gliomas and may facilitate the further identification of novel genetic elements, which may provide us with molecular tools for the improved diagnostics and therapeutic decision-making in these tumors (Roversi et al., 2006). LRP1B has been found frequently mutated in glioblastoma (GBM) (Roversi et al., 2006). A novel internal deletion of LRP1B was discovered in the U118 GBM cell line and four GBM samples. Nucleotide sequencing of the LRP1B gene from U118 cells showed loss of exons 3 to 18 and an early stop codon, suggesting that the protein was no longer functional. This data suggest that LRP1B acts as a tumor suppressor gene in glioma cells and is aberrant in GBM (Yin et al., 2009). |
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Entity | Thyroid cancer |
Note | In non-medullary thyroid cancer, LRP1B under-expression is significantly lower in highly aggressive undifferentiated thyroid tumors (Prazeres et al., 2011). LRP1B expression levels are significantly associated with vascular invasion in follicular thyroid cancer (Prazeres et al., 2011). |
Oncogenesis | Prazeres, Torres et al. (2011) have shown that LRP1B inactivation (by chromosomal, epigenetic and microRNA (miR)-mediated mechanisms) resulted in changes to the tumor environment that confer cancer cells an increased growth and invasive capacity. Restoration of LRP1B impaired in vitro and in vivo tumor growth, inhibited cell invasion and led to a reduction of matrix metalloproteinase 2 in the extracellular medium. This emphasized the role of an endocytic receptor acting as a tumor suppressor by modulating the extracellular environment composition in a way that constrains the invasive behavior of the cancer cells. |
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Entity | Ovarian cancer |
Prognosis | LRP1B binds to fibrinogen and apoE-containing ligands (Haas et al., 2011) and importantly, several studies have suggested that LDL receptor family members are involved in uptake of anionic liposomes and drugs (Chung and Wasan, 2004; Lakkaraju et al., 2002). Due to high degree of intratumoral heterogeneity and the large number of chemotherapeutic agents commonly used in the relapse setting in high-grade serous cancer (HGSC) patients, the most common subtype of ovarian cancer, it is likely that there will be multiple mechanisms of acquired resistance. It was described that the deletion or downregulation of the lipid transporter LRP1B emerged as a significant correlate of acquired resistance. Functional studies showed that reducing LRP1B expression was sufficient to reduce the sensitivity of HGSC cell lines to liposomal doxorubicin, but not to doxorubicin, whereas LRP1B overexpression was sufficient to increase sensitivity to liposomal doxorubicin. These data indicates that LRP1B loss contributes to the emergence of resistance to chemotherapy, specifically to liposomal doxorubicin (Cowin et al., 2012). In conclusion, in high-grade serous ovarian cancers, LRP1B deletion is associated with worse prognosis as a result of acquired chemotherapy resistance to liposomal doxorubicin (Cowin et al., 2012). |
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Entity | Alzheimer's disease |
Note | Initially, LDL receptor gene family was of high interest due to its key function in cholesterol/apolipoprotein E (ApoE) uptake, with the e4 allele of ApoE as the strongest genetic risk factor for late-onset Alzheimer's disease (AD). In a review, Jaeger and Pietrzik (2008) have highlighted the involvement of different lipoprotein receptors in AD. Their functional implications reach from mediating amyloid precursor protein (APP) internalization, as LRP1B, intracellular trafficking, Aβ clearance out of the brain (LRP1) to an involvement in ApoE/cholesterol metabolism. These findings implicate an important role for lipoprotein receptors in the underlying mechanisms leading to the development of AD. These mechanisms will give way to new therapeutic strategies for the treatment of neurodegenerative diseases via interference with the role of lipoprotein receptors. |
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Entity | Atherosclerosis |
Note | Seki, Bujo et al. (2005) have characterized the functions of three groups of cultured smooth muscle cells (SMCs) with different origins in atherosclerotic arteries, in order to know a functional significance of LRP1B in the increased migration of SMCs. The results strongly suggest that LRP1B plays a role in the regulation of migration activity of SMCs through the modification of PDGF signals in the process of atherosclerosis. Tanaga, Bujo et al. (2004) have described that LRP1B modulates the catabolism of uPAR and PDGFR, affecting the migration of smooth muscle cells (SMCs). This functional characterization of LRP1B opens novel avenues for elucidating the (patho)physiological significance of SMC migration in atheromatous plaques. |
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