Golgi phosphoprotein 2 in physiology and in diseases

Kim, Ha-Jeong; Lv, Dandan; Zhang, Yan; Peng, Tao; Ma, Xiaojing

doi:10.1186/2045-3701-2-31

Cited by 36 publications

(32 citation statements)

References 34 publications

(39 reference statements)

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“…GOLM1 has two variants which encode the same protein ( 26 ). Previous studies have demonstrated that the GOLM1 expression is overexpressed in human PCa tissues ( 27 ), HCC ( 28 ), and lung adenocarcinoma ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑143 regulates cell migration and invasion by targeting GOLM1 in cervical cancer

Zhou

Chen

et al. 2018

Oncol Lett

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Accumulated research has revealed that the abnormal expression of microRNAs play a crucial role in tumorigenesis, potentially serving as therapeutic biomarkers in multiple tumors including cervical cancer. However, the expression level, biological role and the underlying mechanism of miRNA-143 in cervical cancer remain unclear. In the current study, we analyzed the miRNA-143 and golgi membrane protein 1 (GOLM1) expression in cervical cancer tissues and cells to explore their effects on cervical cancer occurrence and metastasis. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect the miRNA-143 expression in cervical cancer tissues and cells. Following transfection, cell Transwell assays, western blot analysis and luciferase reporter assays were carried out in human cervical cancer cells. Results demonstrated that the miRNA-143 expression was dramatically decreased in both cervical cancer tissue samples and cells in contrast with the control group. We also found that the miRNA-143 expression negatively correlated with the GOLM1 expression in cervical cancer tissues and miRNA-143 inhibited cell invasion and migration via targeting GOLM1 in cervical cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑143 regulates cell migration and invasion by targeting GOLM1 in cervical cancer

Zhou

Chen

et al. 2018

Oncol Lett

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“…GOLPH2 expression is closely correlated with many diseases (Kim et al, 2012), including hepatocellular carcinoma (Riener et al, 2009), kidney cancer , prostate cancer Wei et al, 2008;Laxman et al, 2008;Roobol et al, 2011), seminoma (Fritzsche et al, 2010), lung adenocarcinoma (Zhang et al, 2010), and others. GOLPH expression was significantly higher in the urine of patients with prostate cancer than in normal controls (Laxman et al, 2008;Roobol et al, 2011), and both the mRNA and protein levels of GOLPH2 were significantly higher than in the normal controls.…”

Section: Discussionmentioning

confidence: 99%

“…Under normal conditions, GOLPH2 is mainly localized in the cis Golgi; however, it can be secreted into the blood through the membrane transport system (Hu et al, 2011). GOLPH2 is a very important biomarker in a variety of diseases (Kim et al, 2012). GOLPH2 was detected in the lesions and sera of patients with liver disease (Riener et al, 2009), and in the lesions of patients with kidney cancer .…”

Section: Introductionmentioning

confidence: 99%

Golgi Phosphoprotein 2 Down-regulates the Th1 Response in Human Gastric Cancer Cells by Suppressing IL-12A

Tang¹,

Ji²,

Tang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Golgi phosphoprotein 2 (GOLPH2) is a very important biomarker in a variety of diseases. Its biological function is not clear, particularly in gastric cancer. To investigate the role of GOLPH2 in human gastric cancer, and determine its effect on the Th1 lymphocyte response, its expression and that of IL-12A were measured by real-time PCR and immunohistochemistry. The relationship between GOLPH2 and IL-12A was analysed statistically. The effect of GOLPH2 on the Th1 lymphocyte response was investigated with an in vitro co-culture system. The results showed that in human gastric cancer, the expression of GOLPH2 was significantly higher and the expression of IL-12A was lower than in normal gastric mucosal tissues, and the expression levels of GOLPH2 and IL-12A were negatively correlated. In addition, obvious down-regulation of the Th1 response was observed when lymphocytes were co-cultured with gastric cancer SGC7901 cells over-expressing GOLPH2. GOLPH2 down-regulated the expression of IL-12A, and inhibited the expression of TNF-α and IFN-γ. The results indicated that GOLPH2 down-regulates the Th1 response via suppression of IL-12A in human gastric cancer, and this might provide a target for the prevention and treatment.

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“…Our analysis indicated that GOLM1-MAK10 could result in the substitution of the last 25 amino acids of GOLM1 by 26 new amino acids and a new 3' UTR from MAK10 (Figure 5A). This would leave the signal peptide and transmembrane domain of GOLM1 intact [16], hence leading to the secretion of an aberrant fusion protein. To investigate this possibility, we cloned the full length ORF of GOLM1-MAK10 and tagged it with a FLAG sequence (Figure 5B), and transfected it in HEK 293T cells.…”

Section: Resultsmentioning

confidence: 99%

Aberrant chimeric RNA GOLM1-MAK10 encoding a secreted fusion protein as a molecular signature for human esophageal squamous cell carcinoma

et al. 2013

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It is increasingly recognized that chimeric RNAs may exert a novel layer of cellular complexity that contributes to oncogenesis and cancer progression, and could be utilized as molecular biomarkers and therapeutic targets. To date yet no fusion chimeric RNAs have been identified in esophageal cancer, the 6th most frequent cause of cancer death in the world. While analyzing the expression of 32 recurrent cancer chimeric RNAs in esophageal squamous cell carcinoma (ESCC) from patients and cancer cell lines, we identified GOLM1-MAK10, as a highly cancer-enriched chimeric RNA in ESCC. In situ hybridization revealed that the expression of the chimera is largely restricted to cancer cells in patient tumors, and nearly undetectable in non-neoplastic esophageal tissue from normal subjects. The aberrant chimera closely correlated with histologic differentiation and lymph node metastasis. Furthermore, we demonstrate that chimera GOLM1-MAK10 encodes a secreted fusion protein. Mechanistic studies reveal that GOLM1-MAK10 is likely derived from transcription read-through/splicing rather than being generated from a fusion gene. Collectively, these findings provide novel insights into the molecular mechanism involved in ESCC and provide a novel potential target for future therapies. The secreted fusion protein translated from GOLM1-MAK10 could also serve as a unique protein signature detectable by standard non-invasive assays. These observations are critical as there is no clinically useful molecular signature available for detecting this deadly disease or monitoring the treatment response.

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Golgi phosphoprotein 2 in physiology and in diseases

Cited by 36 publications

References 34 publications

MicroRNA‑143 regulates cell migration and invasion by targeting GOLM1 in cervical cancer

MicroRNA‑143 regulates cell migration and invasion by targeting GOLM1 in cervical cancer

Golgi Phosphoprotein 2 Down-regulates the Th1 Response in Human Gastric Cancer Cells by Suppressing IL-12A

Aberrant chimeric RNA GOLM1-MAK10 encoding a secreted fusion protein as a molecular signature for human esophageal squamous cell carcinoma

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