Phospholipase A/Acyltransferase enzyme activity of H-rev107 inhibits the H-RAS signaling pathway

Wang, Chunhua; Shyu, Rong-Yaun; Wu, Chang‐Chieh; Tsai, Tzung-Chieh; Wang, Lu-Kai; Chen, Mao-Liang; Jiang, Shun-Yuan; Tsai, Fu-Ming

doi:10.1186/1423-0127-21-36

Cited by 22 publications

(17 citation statements)

References 46 publications

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“…HRASLS3 (H-rev107) was most thoroughly studied in the HRASLS family for suppression of Ras activity. H-rev107 was identified for reversal of H-Ras-derived transformation of rat fibroblasts [98], the PLA/AT activities of HRASLS3 suppress H-Ras signaling [99], and HRASLS3 inhibits K-Ras signaling via a physical association ( Table 2) [100]. HRASLS4 (RIG1, TIG3, RARRES3) suppresses Ras activation [101] and the lung metastasis of breast cancer ( While the mechanisms responsible for FAM84B-derived oncogenesis remain unclear, its direct association with the gene desert as the only other protein coding gene suggests that FAM84B contributes to Myc's oncogenic actions.…”

Section: Potential Collaboration Between Fam84b and Myc During Tumorimentioning

confidence: 99%

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Lin

Kapoor

et al. 2020

Genes

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FAM84B is a risk gene in breast and prostate cancers. Its upregulation is associated with poor prognosis of prostate cancer, breast cancer, and esophageal squamous cell carcinoma. FAM84B facilitates cancer cell proliferation and invasion in vitro, and xenograft growth in vivo. The FAM84B and Myc genes border a 1.2 Mb gene desert at 8q24.21. Co-amplification of both occurs in 20 cancer types. Mice deficient of a 430 Kb fragment within the 1.2 Mb gene desert have downregulated FAM84B and Myc expressions concurrent with reduced breast cancer growth. Intriguingly, Myc works in partnership with other oncogenes, including Ras. FAM84B shares similarities with the H-Ras-like suppressor (HRASLS) family over their typical LRAT (lecithin:retinal acyltransferase) domain. This domain contains a catalytic triad, H23, H35, and C113, which constitutes the phospholipase A 1/2 and O-acyltransferase activities of HRASLS1-5. These enzymatic activities underlie their suppression of Ras. FAM84B conserves H23 and H35 but not C113 with both histidine residues residing within a highly conserved motif that FAM84B shares with HRASLS1-5. Deletion of this motif abolishes FAM84B oncogenic activities. These properties suggest a collaboration of FAM84B with Myc, consistent with the role of the gene desert in strengthening Myc functions. Here, we will discuss recent research on FAM84B-derived oncogenic potential.Genes 2020, 11, 312 2 of 15 non-coding RNA (lnRNA), and on its upstream or centromeric side sits a 1.2 Mb gene desert with the centromeric side bordered by the FAM84B or LRATD2 gene ( Figure 1). The unique feature of this gene desert is the existence of multiple (lnRNAs) (PCAT1, PCAT2, POU5F1B, CCAT1, CCAT2, CASC8, CASC11, CASC19, and CASC21) with FAM84B and Myc being the only protein coding genes (Figure 1) [12][13][14]. In view of Myc being the most-well-studied oncogene and the 8q24 gene desert as a region that is frequently amplified in cancer, FAM84B stands as a promising target for oncogenic activities; nonetheless, its impact on tumorigenesis remained unknown until recently. As the oncogenic potential of the non-coding RNAs of PVT1 and those within the gene desert (Figure 1) has been recently reviewed [13][14][15][16][17], we will focus on the emerging role of FAM84B in tumorigenesis in this review. We will briefly discuss the 8q24 gene desert with respect to oncogenesis to set the stage for the following systemic examination of the evidence pertinent to FAM84B-derived tumorigenesis. The main materials used in this review were chosen based on the PRISMA (preferred reporting items for systematic reviews and meta-analyses) Guidelines [18,19]. A literature search of the PubMed database for (1) "8q24 gene desert", revealed 28 papers with 6 irrelevant to tumorigenesis (Figure 2A) and (2) "FAM84B", identified 21 articles, including non-English papers (n = 1) and articles not directly related to FAM84B and cancer (n = 2) ( Figure 2B). After excluding these items, 22 articles on 8q24 gene desert and 18 papers related to the FAM84B topic h...

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Section: Potential Collaboration Between Fam84b and Myc During Tumorimentioning

confidence: 99%

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Lin

Kapoor

et al. 2020

Genes

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“…Such a model should account for various modeling elements that include: a) a nucleation and variant selection criterion; b) the introduction of martensitic grains in the aggregate; c) the orientation relationship between the martensitic grain and its parent austenitic phase; d) the evolution of the martensitic grain and the implementation of the martensitic phase transformation strain. In this work, those modeling elements are incorporated into the elastic viscoplastic self-consistent (EVPSC) model [14,[22][23][24][25][26]. The EVPSC model has been successfully applied to study the evolution of internal elastic strain of stainless steel not exhibiting transformation [14,27], magnesium alloys [28][29][30] and zirconium alloys [31].…”

Section: Introductionmentioning

confidence: 99%

Effect of martensitic phase transformation on the behavior of 304 austenitic stainless steel under tension

Wang

Jeong

Clausen

et al. 2016

Materials Science and Engineering: A

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The present work integrates in-situ neutron diffraction, electron backscatter diffraction and crystal plasticity modeling to investigate the effect of martensitic phase transformation on the behavior of 304 stainless steel under uniaxial tension. The macroscopic stress strain response, evolution of the martensitic phase fraction, texture evolution of each individual phase, and internal elastic strains were measured at room temperature and at 75°C. Because no martensitic transformation was observed at 75°C, the experimental results at 75°C were used as a reference to quantify the effect of formed martensitic phase on the behavior of 304 stainless steel at room temperature. A crystallographic phase transformation model was implemented into an elasticviscoplastic self-consistent framework. The phase transformation model captured the macroscopic stress strain response, plus the texture and volume fraction evolution of austenite and martensite. The model also predicts the internal elastic strain evolution with loading in the austenite, but not in the martensite. The results of this work highlight the mechanisms that control phase transformation and the sensitivity of modeling results to them, and point out to critical elements that still need to be incorporated into crystallographic phase transformation models to accurately describe the internal strain evolution during phase transformation.

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“…PLA2G16 inhibits the growth of ovarian carcinoma (5), cervical (17) and testicular carcinoma cell (10). It was also reported that J Thorac Dis 2017;9(4):1002-1011 jtd.amegroups.com …”

Section: Discussionmentioning

confidence: 95%

“…PLA2G16 is first identified as a tumor suppressor to inhibit HRAS induced transformation, cell proliferation, colony formation, and promote apoptosis (8,9,22,23). PLA2G16 exerts its anti-RAS activity through its PLA/AT activity to decrease the steady state levels of H-RAS palmitoylation in cervical cancer cells (17) and the suppression of RAS by © Journal of Thoracic Disease. All rights reserved.…”

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High expression of PLA2G16 is associated with a better prognosis in HER2-positive breast cancer

et al. 2017

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Background: PLA2G16 functions as a phosphatase in metabolism and its abnormal expression is closely associated with tumor progression. The aim of this study is to investigate the prognosis value of PLA2G16 in breast cancer. Methods: A tissue microarray including 200 invasive ductal carcinoma specimens was constructed.Immunohistochemistry was performed to determine the PLA2G16 expression status. The Kaplan-Meier analysis and log-rank test were used to evaluate the prognostic value of PLA2G16. The Multivariate Cox regression analysis was performed to identify whether PLA2G16 was an independent prognostic factor. Results: In our retrospective study, Kaplan-Meier analysis showed that elevated PLA2G16 expression was correlated with improved DFS (P=0.032) in the whole breast cancer patients. In further subgroup analysis, PLA2G16 overexpression was found to be associated with prolonged DFS (P=0.018) in HER2-positive breast cancer patients. More importantly, Multivariate analysis suggested that PLA2G16 was a significant independent prognostic factor in HER2-enriched patients [hazard ratio (HR) =0.151; 95% confidence interval (CI) =0.034-0.672; P=0.013]. Conclusions: Our study evaluated the prognostic significance of PLA2G16 in patients with HER2-positive breast cancer and confirmed the relevance of this metabolism-related gene in patient outcome.

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Phospholipase A/Acyltransferase enzyme activity of H-rev107 inhibits the H-RAS signaling pathway

Cited by 22 publications

References 46 publications

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Effect of martensitic phase transformation on the behavior of 304 austenitic stainless steel under tension

High expression of PLA2G16 is associated with a better prognosis in HER2-positive breast cancer

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