Olfactomedin-like 2 A and B (OLFML2A and OLFML2B) expression profile in primates (human and baboon)

Pérez-Ibave, Diana Cristina; González-Álvarez, Rafael; Martínez‐Fierro, Margarita L.; Ruiz-Ayma, Gabriel; Luna-Muñoz, Maricela; Martínez-de-Villarreal, Laura Elia; Garza‐Rodríguez, María Lourdes; Reséndez‐Pérez, Diana; Mohamed-Noriega, Jibran; Garza‐Guajardo, Raquel; Bautista-De-Lucío, Víctor Manuel; Mohamed-Noriega, Karim; Barboza-Quintana, Oralia; Arámburo, Carlos; Barrera-Saldaña, Hugo A.; Rodríguez‐Sánchez, Iram P.

doi:10.1186/s40659-016-0101-8

Cited by 14 publications

(17 citation statements)

References 26 publications

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“…But, the potential ability and detailed mechanism of RERG in gastric cancer requires further study. OLFML2B, located on chromosome 1q23.3, was first identified and characterized in mouse retina [32,33]. In gastric cancer, OLFML2B could promote the growth of gastric cancer cells, maybe serving an oncogene in the development of gastric cancer [34].…”

Section: Discussionmentioning

confidence: 99%

Identification of prognosis-related genes in the tumor microenvironment of stomach adenocarcinoma by TCGA and GEO datasets

Ren

Liang

2020

Bioscience Reports

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Accumulating evidence has demonstrated that tumor microenvironment (TME) plays a crucial role in stomach adenocarcinoma (STAD) development, progression, prognosis and immunotherapeutic responses. How the genes in TME interact and behave is extremely crucial for tumor investigation. In the present study, we used gene expression data of STAD available from TCGA and GEO datasets to infer tumor purity using ESTIMATE algorithms, and predicted the associations between tumor purity and clinical features and clinical outcomes. Next, we calculated the differentially expressed genes (DEGs) from the comparisons of immune and stromal scores, and postulated key biological processes and pathways that the DEGs mainly involved in. Then, we analyzed the prognostic values of DEGs in TCGA dataset, and validated the results by GEO dataset. Finally, we used CIBERSORT computational algorithm to estimate the 22 tumor infiltrating immune cells (TIICs) subsets in STAD tissues. We found that stromal and immune scores were significantly correlated with STAD subtypes, clinical stages, Helicobacter polyri infection, and stromal scores could predict the clinical outcomes in STAD patients. Moreover, we screened 307 common DEGs in TCGA and GSE51105 datasets. In the prognosis analyses, we only found OGN, JAM2, RERG, OLFML2B, and ADAMTS1 genes were significantly associated with overall survival in TCGA and GSE84437 datasets, and these genes were correlated with the fractions of T cells, B cells, macrophages, monocytes, NK cells and DC cells, respectively. Our comprehensive analyses for transcriptional data not only improved the understanding of characteristics of TME, but also provided the targets for individual therapy in STAD.

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Section: Discussionmentioning

confidence: 99%

Identification of prognosis-related genes in the tumor microenvironment of stomach adenocarcinoma by TCGA and GEO datasets

Ren

Liang

2020

Bioscience Reports

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“…SPRY4 has a known role in inhibiting the Ras pathway, and its family member SPRY2 is also up‐regulated in our study and another, thus indicating that this family may be involved in NF1 signaling. OLFML2A is expressed in the eye and kidney podocyte; the relevance to NF1 remains to be determined . It has been suggested that based on the olfactomedin domain within OLFML2A, it may bind neurofascin, and along with doublecortin may serve to stabilize microtubular structures …”

Section: Resultsmentioning

confidence: 99%

Multi‐Omics Profiling for NF1 Target Discovery in Neurofibromin (NF1) Deficient Cells

et al. 2019

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Loss of NF1 is an oncogenic driver. In efforts to define pathways responsible for the development of neurofibromas and other cancers, transcriptomic and proteomic changes are evaluated in a non-malignant NF1 null cell line. NF1 null HEK293 cells were created using CRISPR/Cas9 technology and they are compared to parental cells that express neurofibromin. A total of 1222 genes and 132 proteins are found to be differentially expressed. The analysis is integrated to identify eight transcripts/proteins that are differentially regulated in both analyses. Metacore Pathway analysis identifies Neurogenesis NGF/TrkA MAPK-mediated signaling alterations. Next, the data set is compared with other published studies that involve analysis of cells or tumors deficient for NF1 and it is found that 141 genes recur in the sample and others; only thirteen of these genes recur in two or more studies. Genes/proteins of interest are validated via q-RT-PCR or Western blot. It is shown that KRT8 and 14-3-3σ protein levels respond to exogenously introduced mNf1 cDNA. Hence, transcripts/proteins that respond to neurofibromin levels are identified and they can potentially be used as biomarkers.deletions, duplications, splicing variants, and rearrangements. Neurofibromin is best characterized by its ability to interact with and inactivate Ras through its GAP related domain (GRD). Hyperactivation of the Ras signaling pathway results in cellular over-proliferation and tumor formation. As such, NF1 is one of several disorders termed "Rasopathies," which also include Noonan syndrome, Costello syndrome, Legius syndrome, and others.Neurofibromin functions as a tumor suppressor. Inactivation of NF1 is sufficient for neurofibroma initiation. [1] Germline NF1 mutations have been associated with an earlier age of onset for breast cancer. Somatic mutations are present in tumors associated with NF1 and in a range of sporadic tumors in different cell types such as glioblastoma (up to 23%), lung adenocarcinoma (up to 11.8%), and breast cancer (reviewed in ref. 2). About 10-14% of children with juvenile myelomonocytic leukemia (JMML) have a clinical diagnosis of NF1 and NF1 mutations occur in approximately 30% of JMML cases. [3] This implies an important role for neurofibromin function in cancer development and progression.Since 2005, there have been at least fifteen studies utilizing sequencing, transcriptomics, and proteomics to discover factors important to NF1 pathology; these are summarized in Table S1, Supporting Information. [1,[4][5][6][7][8][9][10][11][12][13] One study looked only at whole exome sequencing, [10] two studies evaluated sequencing and transcriptomics, [1,8] nine were transcriptomic studies, [4,5,[11][12][13] two were proteomics studies with mouse tissues, [6,7] and one was a transcriptomic and proteomic study done after Nf1 siRNA treatment in rat cells. [9] These studies highlighted different drivers of NF1 pathology and took advantage of both mouse and human sources as well as a variety of cell types, including neurons, induced-n...

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“…Data obtained over the past several years demonstrate that OLF family proteins play important roles in neurogenesis, neural crest formation, dorsal ventral patterning, cell-cell adhesion, cell cycle regulation, and tumorigenesis and may act as modulators of critical signaling pathways (Wnt, BMP) [7]. Human OLFML2A genes are located on chromosome 9q33.3 and encode secreted glycoproteins also known as photomedin-1 [9]. The biological functions of proteins that possess the OLF domain remain elusive [7,9,21].…”

Section: Discussionmentioning

confidence: 99%

“…Human OLFML2A genes are located on chromosome 9q33.3 and encode secreted glycoproteins also known as photomedin-1 [9]. The biological functions of proteins that possess the OLF domain remain elusive [7,9,21]. In the eld of cancer research, the tumorigenic function of OLFM4 has been veri ed in many tumors [22,23].…”

Section: Discussionmentioning

confidence: 99%

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OLFML2A Downregulation Inhibits Glioma Proliferation Through Suppression of Wnt/β-Catenin Signaling

Duan

Dong

et al. 2020

Preprint

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Background: Glioma is a highly heterogeneous and lethal tumor with extremely poor prognosis. Through analysis of TCGA data, we found that OLFML2A was significantly upregulated in glioma tissues and positively correlated with glioma grade and worse prognosis. However, the molecular function of OLFML2A and its underlying mechanism in glioma remain unclear.Methods: The expression of OLFML2A in glioma was determined by immunohistochemistry (IHC). Celigo assay, MTT assay and flow cytometry were utilized to evaluate the effects of OLFML2A on glioma proliferation and apoptosis. Gene chip microarray analysis and ingenuity pathway analysis were used to investigate the potential regulatory mechanisms of OLFML2A, which were further assessed by q-PCR, western blotting and IHC. An animal transplanting glioma model and spectral computed tomography scan were used to verify OLFML2A expression in vivo.Results: In this study, we found that the expression of OLFML2A was significantly upregulated in glioma specimens and positively correlated with pathological grades in glioma patients. Moreover, Kaplan-Meier survival analysis of TCGA data revealed that glioma patients with higher expression of OLFML2A had shorter overall survival. Importantly, when we knocked down the expression of OLFML2A in glioma cells, cell proliferation was inhibited, and apoptosis was promoted. Mechanistically, downregulation of OLFML2A inhibited Wnt/β-catenin signaling by directly reducing the level of stabilized β-catenin and upregulating the expression of amyloid precursor protein (APP) to indirectly suppress β-catenin, leading to repression of MYC, CD44 and CSKN2A2 expression. Furthermore, we found that OLFML2A downregulation clearly suppressed the growth of subcutaneous glioma and intracranial transplantation of glioma by inhibiting Wnt/β-catenin pathway-dependent cell proliferation.Conclusion: Our data indicate the oncogenic effect of OLFML2A in glioma through regulation of Wnt/β-catenin signaling, which may provide a novel therapeutic target for glioma.

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Olfactomedin-like 2 A and B (OLFML2A and OLFML2B) expression profile in primates (human and baboon)

Cited by 14 publications

References 26 publications

Identification of prognosis-related genes in the tumor microenvironment of stomach adenocarcinoma by TCGA and GEO datasets

Identification of prognosis-related genes in the tumor microenvironment of stomach adenocarcinoma by TCGA and GEO datasets

Multi‐Omics Profiling for NF1 Target Discovery in Neurofibromin (NF1) Deficient Cells

OLFML2A Downregulation Inhibits Glioma Proliferation Through Suppression of Wnt/β-Catenin Signaling

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