Computational Analysis on the Role of GPM6A in Human Thyroid Cancer

Khalid, Zoya; Sameen, Sheema; Malik, Shaukat Iqbal; Shehzad, Sheeba

doi:10.4172/2153-0602.1000114

Cited by 3 publications

(4 citation statements)

References 27 publications

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“…Furthermore, higher expression of GPM6A was observed in poorly differentiated colorectal cancers compared with highly differentiated cancers 23,24 . Papillary thyroid carcinomas express higher levels of GPM6A compared with normal thyroid tissue 25 . In primary B‐cell malignancies induced by the Graffi mouse leukemia virus in mice, GPM6A was also found to be overexpressed 22 .…”

Section: Discussionmentioning

confidence: 97%

Glycoprotein M6A upregulation detected by transcriptome analysis controls the proliferation of keloidal fibroblasts

Kurimoto‐Nishiguchi,

Muraoka,

Inaba

et al. 2023

The Journal of Dermatology

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Hypertrophic scars and keloids are fibroproliferative disorders caused by abnormal wound healing. Their exact cause has not been found, but abnormalities during the wound healing process including inflammatory, immune, genetic, and other factors are thought to predispose an individual to excessive scarring. In the present study, we performed transcriptome analysis of established keloid cell lines (KEL FIB), focusing on gene expression analysis and fusion gene detection for the first time. For gene expression analysis, fragments per kilobase per million map read values were calculated, which were validated by real‐time PCR and immunohistochemistry. Fusion genes were predicted by transcriptome sequence, and validated by Sanger sequence and G‐banding. As a result, GPM6A was shown in the expression analysis to be upregulated in KEL FIB compared with normal fibroblasts. The GPM6A upregulation in KEL FIB was confirmed by real‐time PCR, and GPM6A messenger ribonucleic acid expression was consistently significantly elevated in the tissues of hypertrophic scar and keloid compared to normal skin. Immunohistochemistry also revealed that the number of fibroblast‐like spindle‐shaped cells positive for GPM6A was significantly increased in keloidal tissues. GPM6A inhibition by small interfering ribonucleic acid significantly reduced the number of KEL FIB. On the other hand, although we hypothesized that fusion genes are involved in the pathogenesis of keloids, the transcriptome analysis could not prove the presence of fusion genes in KEL FIB. Taken together, GPM6A upregulation may have an inducible effect on cell proliferation in keloidal fibroblasts. GPM6A can be a novel therapeutic target in hypertrophic scars and keloids. The inflammatory nature may be more prominent in the pathogenesis of keloids, rather than being skin tumors, as proposed by Ogawa et al. Future studies using several cell lines will be required.

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Section: Discussionmentioning

confidence: 97%

Glycoprotein M6A upregulation detected by transcriptome analysis controls the proliferation of keloidal fibroblasts

Kurimoto‐Nishiguchi,

Muraoka,

Inaba

et al. 2023

The Journal of Dermatology

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“…GPM6A has been described as differentially expressed in thyroid cancer, expressed at higher levels in papillary thyroid carcinoma as compared to normal thyroid tissue 16 . In primary B-cell malignancies induced by Graffi murine leukemia virus in mice, GPM6A was found to be over-expressed; ectopic expression of GPM6A in NIH 3T3 cells promoted cell proliferation and anchorage-independent cell growth in vitro 17 .…”

Section: Discussionmentioning

confidence: 99%

Glycoprotein M6A is differentially expressed in non-small cell lung cancer and associates with patient survival.

Mamoor¹

2020

Preprint

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Non-small cell lung cancer (NSCLC) is the leading cause of cancer death in the United States (1). We mined published microarray data (2, 3, 4) to identify differentially expressed genes in NSCLC. We found that gene encoding glycoprotein M6A, GPM6A, was among those whose expression was most quantitatively different in human NSCLC tumors as compared to the lung. GPM6A expression levels were significantly decreased in NSCLC tumors as compared to the lung, and lower expression of GPM6A in patient tumors was significantly associated with worse overall survival. GPM6A may be important for initiation or progression of non-small cell lung cancer in humans.

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“…They found increased BAFF mRNA expression and concluded that the increase is not reflective of histological disease severity. A review article by Khalid et al [6] presents an overview of therapeutic use of retinoids, a group of natural and synthetic derivatives of vitamin A for LN. The review discusses the details of LN pathogenesis and severity in humans, and current and new agents for the treatment.…”

mentioning

confidence: 99%

“…Computational analysis of microarray data and serial analysis of gene expression enabled Khalid et al [6] to show that the protein GPM6A plays a major role in cell migration and is a major contributor in tumor formation. The results could lead to earlier diagnosis and better treatment for thyroid cancer patients.…”

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confidence: 99%

Highlights of Recent Articles on Data Mining in Genomics and Proteomics

Natarajan¹

2013

J Data Mining in Genom Proteomics

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Computational Analysis on the Role of GPM6A in Human Thyroid Cancer

Cited by 3 publications

References 27 publications

Glycoprotein M6A upregulation detected by transcriptome analysis controls the proliferation of keloidal fibroblasts

Glycoprotein M6A upregulation detected by transcriptome analysis controls the proliferation of keloidal fibroblasts

Glycoprotein M6A is differentially expressed in non-small cell lung cancer and associates with patient survival.

Highlights of Recent Articles on Data Mining in Genomics and Proteomics

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