Critical regions and spreading of runt-related transcription factor-3 C-phosphate-G (CpG) island methylation in human salivary gland adenoid cystic carcinoma

Ge, Minghua; Chen, Chao; Xu, Jiajie; Ling, Zhi‐Qiang

doi:10.1016/j.humpath.2011.02.003

Cited by 14 publications

(18 citation statements)

References 28 publications

(35 reference statements)

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“…Total protein was extracted and then quantified using the Lowry method. 39 Western blot analysis was performed using anti-PDCD4, anti-total STAT3, and antiphospho-STAT3 monoclonal antibodies according to the previous report 9 and normalized to GAPDH (Abcam, Cambridge) protein expression. (Figure 1a).…”

Section: Construction Of Expression Vectorsmentioning

confidence: 99%

“…4,5 Although the 5-year survival rate is high for patients with SACC, probably because of the slow growth of the tumor, the 10-and 15-year prognoses are poor because of the frequent local recurrences and distant metastases. [6][7][8] Although multiple genetic and epigenetic alterations have been detected in SACC, 3,[9][10][11][12][13] the precise molecular mechanisms of progression and metastasis of SACC remain unknown.…”

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confidence: 99%

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miR-21 regulates tumor progression through the miR-21-PDCD4-Stat3 pathway in human salivary adenoid cystic carcinoma

Jiang

Hou

et al. 2015

Laboratory Investigation

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miR-21, which is a putative tumor onco-miR and frequently overexpressed microRNA in various tumors, has been linked to tumor progression through targeting of tumor-suppressor genes. In this study, we sought to determine whether miR-21 has any role on tumor progression of salivary adenoid cystic carcinoma (SACC) and the possible mechanisms. We found that the level of miR-21 expression was significantly higher in SACC than that in normal salivary tissues, and it is also higher in tumors with metastasis than that without metastasis. Using an anti-miR-21 inhibitor in an in vitro model, downregulation of miR-21 significantly decreased the capacity of invasion and migration of SACC cells, whereas a pre-miR-21 increased the capacity of invasion and migration of SACC cells. To explore the potential mechanisms by which miR-21 regulate invasion and migration, we identified one direct miR-21 target gene, programmed cell death 4 (PDCD4), which has been implicated in invasion and metastasis Salivary adenoid cystic carcinoma (SACC) is one of the most common malignancy of the salivary gland, accounting for 10% of salivary gland tumors and 30% of human salivary gland malignancies. 1,2 SACC is characterized by slow but aggressive growth, nerve and blood vessel invasion, multiple recurrences, and distant metastases. 3-5 Lung metastasis and nerve metastasis are the biological characteristics of SACC. [6][7][8] It has been reported that the incidence of SACC with distant metastasis ranged from 35 to 50% of all cases. Lung was the most common organ of its distant metastasis, and lung metastasis is still the leading death cause of patients with SACC. 4,5 Although the 5-year survival rate is high for patients with SACC, probably because of the slow growth of the tumor, the 10-and 15-year prognoses are poor because of the frequent local recurrences and distant metastases. [6][7][8] Although multiple genetic and epigenetic alterations have been detected in SACC, 3,9-13 the precise molecular mechanisms of progression and metastasis of SACC remain unknown.MicroRNAs (miRNAs) are small non-coding RNA molecules, with a length of 20-22 nucleotides, that regulate gene expression by either translational inhibition or mRNA degradation. miRNAs function as either oncogenes or tumor suppressors by inhibiting the expression of target genes, some of which are either directly or indirectly involved with canonical signaling pathways. 13,14 The roles and function of some selected miRNAs in SACC have been reported. 15

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Section: Construction Of Expression Vectorsmentioning

confidence: 99%

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confidence: 99%

miR-21 regulates tumor progression through the miR-21-PDCD4-Stat3 pathway in human salivary adenoid cystic carcinoma

Jiang

Hou

et al. 2015

Laboratory Investigation

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“…Consistent with previous findings, the present study demonstrated vimentin overexpression in GC cell lines and clinical GC tissues. Over the past decade, knowledge of the importance of epigenetic events in the control of normal cellular processes, and aberrant events leading to tumor development and progression has increased (3)(4)(5)(6)(7)22). DNA methylation is a major epigenetic mechanism that has been intensively investigated in the context of gene regulation and abnormal gene silencing in cancer cells (3)(4)(5)(6).…”

Section: Discussionmentioning

confidence: 99%

“…Over the past decade, knowledge of the importance of epigenetic events in the control of normal cellular processes, and aberrant events leading to tumor development and progression has increased (3)(4)(5)(6)(7)22). DNA methylation is a major epigenetic mechanism that has been intensively investigated in the context of gene regulation and abnormal gene silencing in cancer cells (3)(4)(5)(6). DNA methylation-associated biomarkers are under investigation in various types of human cancer (3)(4)(5)7).…”

Section: Discussionmentioning

confidence: 99%

“…Gastric tumorigenesis is a complex, multi-step process involving alterations of numerous genes (2). Aberrant promoter methylation is an important mechanism for silencing certain tumor suppressor and tumor-associated genes, and is significant during the pathogenesis and progression of certain types of human cancer (3,4), including GC (5,6). Data suggests that DNA methylation may be a useful biomarker for cancer risk evaluation (3,5), early diagnosis (5), prognosis (4,5) and evaluation of sensitivity to chemotherapy (7).…”

Section: Introductionmentioning

confidence: 99%

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DNA hypermethylation of the vimentin gene inversely correlates with vimentin expression in intestinal- and diffuse-type gastric cancer

et al. 2015

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Abstract. T he vimentin gene is a hallma rk of epithelial-to-mesenchymal transition and has been observed to be overexpressed in various types of tumor cell line and tissue. Previous studies have reported correlations between vimentin DNA methylation levels and subsequent vimentin expression levels in solid tumors, including breast and colorectal cancer; however, to the best of our knowledge, such a correlation has not been reported for gastric cancer (GC) using Lauren classification. Therefore, the present study aimed to quantify DNA methylation levels of the vimentin gene using quantitative (q) methylation-specific polymerase chain reaction (PCR) in intestinal-type GC cell lines (MKN-28, AGS and MKN-1), diffuse-type GC cell lines (SGC-7901, SNU-5 and KATO III), the GES-1 immortalized human non-neoplastic gastric epithelial cell line, as well as in tumor and paratumor normal tissue samples. Furthermore, the present study analyzed the messenger RNA expression of the vimentin gene in these cell lines and tissues by reverse transcription-qPCR. A comparison of the clinicopathological features was conducted between patients, grouped according to the Lauren classification. The present study identified that the vimentin promoter region was hypermethylated in all GC cell lines and tumor tissue samples when compared with immortalized normal gastric epithelial cells and paratumor normal tissues. In addition, vimentin promoter methylation levels were observed to be higher in intestinal-type cell lines when compared with those of diffuse-type lines and tissues. Correspondingly, vimentin expression levels were lower in intestinal-type gastric cell lines compared with those of diffuse-type cell lines and tissues, and were lowest in the non-neoplastic gastric cell line and paratumor normal tissues. Patients with diffuse-type GC were on average younger (P=0.023), and exhibited higher tumor (P=0.020), node (P= 0.032) and TNM classification of malignant tumor stage (P=0.039) than those with intestinal-type GC. Following treatment of AGS cells (which demonstrated the highest methylation level of the vimentin gene) with 5-aza-2'-deoxycytidine, vimentin expression was restored significantly. Thus, the present study revealed that vimentin promoter methylation levels are inversely correlated with vimentin expression levels in GC (according to Lauren classification). High levels of methylation in the vimentin gene promoter region may be involved in carcinogenesis and the development of GC, and may provide a novel molecular classification for GC.

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Down-Regulation of PTEN Expression Modulated by Dysregulated miR-21 Contributes to the Progression of Esophageal Cancer

Mao

Zheng

et al. 2013

Dig Dis Sci

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Critical regions and spreading of runt-related transcription factor-3 C-phosphate-G (CpG) island methylation in human salivary gland adenoid cystic carcinoma

Cited by 14 publications

References 28 publications

miR-21 regulates tumor progression through the miR-21-PDCD4-Stat3 pathway in human salivary adenoid cystic carcinoma

miR-21 regulates tumor progression through the miR-21-PDCD4-Stat3 pathway in human salivary adenoid cystic carcinoma

DNA hypermethylation of the vimentin gene inversely correlates with vimentin expression in intestinal- and diffuse-type gastric cancer

Down-Regulation of PTEN Expression Modulated by Dysregulated miR-21 Contributes to the Progression of Esophageal Cancer

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