Overexpression of MICAL2, a novel tumor-promoting factor, accelerates tumor progression through regulating cell proliferation and EMT

Cai, Yingfan; Lu, Jinping; Tang, Faqing

doi:10.7150/jca.22355

Cited by 33 publications

(28 citation statements)

References 58 publications

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“…Our previous work has reported that MICAL2 is the major regulator of breast cancer cell migration through inhibiting EGFR/P38 signalling activation . In the current study, we further extended our observation on MICAL‐L2 that lacks flavoprotein monooxygenase (MO) domain and owns C‐terminal domains (CTD) compared with MICAL2 . We showed that gastric cancer cell migrative potential was greatly impaired, which was likely mediated by the knockdown of MICAL‐L2 expression, whereas overexpression of MICAL‐L2 increased cell motility.…”

Section: Discussionsupporting

confidence: 69%

MICAL‐L2 potentiates Cdc42‐dependent EGFR stability and promotes gastric cancer cell migration

Min

Zhao

Liu

et al. 2019

J Cellular Molecular Medi

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Enhanced migration potential is a common characteristic of cancer cells induced by mechanisms that are incompletely defined. The present study was designed to investigate relationship of a new discovered cytoskeleton regulator MICAL‐L2 and the endogenous epidermal growth factor receptor (EGFR) signalling pathways in gastric cancer cell migration. Increased expression of MICAL‐L2 in gastric cancer cells up‐regulated EGFR protein level, accompanied by the increase of cell migration, whereas silencing MICAL‐L2 down‐regulated EGFR and inhibited cell migration. Expression of MICAL‐L2 was also shown positively correlated with the activation of HSP27/cytoskeleton and HSP27/β‐catenin signalling pathways that provide key mechanisms controlling cell migration. The up‐regulating effect of MICAL‐L2 on EGFR is mediated through a transcription‐independent mechanism that involves inhibiting EGFR protein degradation in lysosome. Further analysis indicated that Cdc42 activation contributed in maintaining the effect of MICAL‐L2 on EGFR stability. Furthermore analysis of clinic specimens revealed increased expression of MICAL‐L2 in carcinoma tissues and a positive correlation between MICAL‐L2 and EGFR expression levels. The above results indicate that MICAL‐L2 potentiates gastric cell migration via inhibiting EGFR degradation in lysosome via a Cdc42‐dependent manner that leads to the activation of EGFR/HSP27 signalling pathways.

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Section: Discussionsupporting

confidence: 69%

MICAL‐L2 potentiates Cdc42‐dependent EGFR stability and promotes gastric cancer cell migration

Min

Zhao

Liu

et al. 2019

J Cellular Molecular Medi

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“…Molecule interacting with CasL (MICAL2), a microtubule associated monooxygenase, is involved in cell growth, axon guidance, vesicle trafficking and apoptosis. Recent studies have demonstrated that MICAL2 is highly expressed in tumor and accelerates tumor progression and it is deemed to be a novel tumor-promoting factor [48,49]. PCSK5 belongs to the subtilisin-like proprotein convertase family.…”

Section: Discussionmentioning

confidence: 99%

A methylation‐based mRNA signature predicts survival in patients with gastric cancer

Sun

Zhang

et al. 2020

Cancer Cell Int

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Background: Evidence suggests that altered DNA methylation plays a causative role in the occurrence, progression and prognosis of gastric cancer (GC). Thus, methylated-differentially expressed genes (MDEGs) could potentially serve as biomarkers and therapeutic targets in GC. Methods: Four genomics profiling datasets were used to identify MDEGs. Gene Ontology enrichment and Kyoto Encyclopaedia of Genes and Genomes pathway enrichment analysis were used to explore the biological roles of MDEGs in GC. Univariate Cox and LASSO analysis were used to identify survival-related MDEGs and to construct a MDEGs-based signature. The prognostic performance was evaluated in two independent cohorts. Results: We identified a total of 255 MDEGs, including 192 hypermethylation-low expression and 63 Hypomethylation-high expression genes. The univariate Cox regression analysis showed that 83 MDEGs were associated with overall survival. Further we constructed an eight-MDEGs signature that was independent predictive of prognosis in the training cohort. By applying the eight-MDEGs signature, patients in the training cohort could be categorized into high-risk or low-risk subgroup with significantly different overall survival (HR = 2.62, 95% CI 1.71-4.02, P < 0.0001). The prognostic value of the eight-MDEGs signature was confirmed in another independent GEO cohort (HR = 1.35, 95% CI 1.03-1.78, P = 0.0302) and TCGA-GC cohort (HR = 1.85, 95% CI 1.16-2.94, P = 0.0084). Multivariate cox regression analysis proved the eight-MDEGs signature was an independent prognostic factor for GC. Conclusion: We have thus established an innovative eight-MDEGs signature that is predictive of overall survival and could be a potentially useful guide for personalized treatment of GC patients.

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“…The nine leading edge genes (Table 1) in GO: 0016705 had various roles ranging from cell proliferation (MICAL2) [46] to encoding enzymes for proper peroxisome function (PYPH) [47]. Four leading edge genes influence the ovarian (DBH, MICAL2, CYP19A1) and uterine environments (PTGS1), while one (HMOX1) is involved in the immune response ( Table 1).…”

Section: Plos Onementioning

confidence: 99%

Loci associated with conception rate in crossbred beef heifers

et al. 2020

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The inability of beef cattle to maintain full term pregnancies has become an economic concern for the beef industry. Herd management and nutritional improvements have alleviated environmental impacts on embryonic and fetal loss, yet additional gains can be made through genomic selection. The objectives of this study were to identify loci and gene-sets in crossbred beef heifers associated with the number of services required to become pregnant (TBRD) and heifer conception rate at first service (HCR1). Heifers (n = 709) from a commercial beef operation underwent one round of artificial insemination, before exposure to bulls for natural service for 50 days. Pregnancy and time of conception was determined by ultrasound 35 days after the breeding season. Heifers were genotyped using the GeneSeek (Lincoln, NE) Bovine GGP50K BeadChip prior to genome-wide association analyses (GWAA) conducted using an EIGENSTRAT-like model to identify loci associated (P < 1 × 10 −5) with TBRD and HCR1. One locus was associated (P = 8.97 × 10 −6) with TBRD on BTA19 and included the positional candidate gene ASIC2, which is differentially expressed in the endometrium of fertility classified heifers, and the positional candidate gene, SPACA3. Gene-set enrichment analyses using SNP (GSEA-SNP) data, was performed and identified one gene-set, oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen as enriched (NES = 3.15) with TBRD and contained nine leading edge genes that contributed to the enrichment of the gene set. The enriched gene-set is involved in catalyzing oxidation-reduction reactions, which have been associated with oxidative stressors impacting pregnancy success. No loci were associated nor gene-sets enriched with HCR1. Identification of loci, positional candidate genes, gene-sets and leading edge genes enriched for fertility facilitate genomic selection that allows producers to select for reproductively superior cattle, reduce costs associated with infertility, and increase percent calf crop.

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Overexpression of MICAL2, a novel tumor-promoting factor, accelerates tumor progression through regulating cell proliferation and EMT

Cited by 33 publications

References 58 publications

MICAL‐L2 potentiates Cdc42‐dependent EGFR stability and promotes gastric cancer cell migration

MICAL‐L2 potentiates Cdc42‐dependent EGFR stability and promotes gastric cancer cell migration

A methylation‐based mRNA signature predicts survival in patients with gastric cancer

Loci associated with conception rate in crossbred beef heifers

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