Correlation between histone acetylation and expression of the <i>MYO18B</i> gene in human lung cancer cells

Tani, Masachika; Ito, Jun itsu; Nishioka, Michiho; Kohno, Takashi; Tachibana, Kunihide; Shiraishi, Masahiko; Takenoshita, Seiichi; Yokota, Jun

doi:10.1002/gcc.20027

Cited by 32 publications

(25 citation statements)

References 19 publications

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“…However, MYO18A was not overexpressed in prostate cancer tissues, and so far has not been associated with other cancers. In contrast, MYO18B, has been identified as a tumour suppressor gene, with loss of expression, deletions and/or mutations reported for a lung cancer cell line, and malignant pleural mesothelioma [64] as well as ovarian [65] and other lung cancers [57,66], melanoma and pancreatic carcinoma [67]. Restoration of MYO18B expression in the lung cancer cell line H1299 inhibited anchorage independent growth and motility through an interaction with HOMER2 [58].…”

Section: Myo9b and Myo18a Modulators Of Nm2 Filament Organisationmentioning

confidence: 99%

How myosin organization of the actin cytoskeleton contributes to the cancer phenotype

Peckham

2016

Biochemical Society Transactions

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The human genome contains 39 genes that encode myosin heavy chains, classified on the basis of their sequence similarity into 12 classes. Most cells express at least 12 different genes, from at least 8 different classes, which are typically composed of several class 1 genes, at least one class 2 gene, and classes 5, 6, 9, 10, 18 and 19. While the different myosin isoforms all have specific and non-overlapping roles in the cell, in combination they all contribute to the organisation of the actin cytoskeleton, and the shape and phenotype of the cell. Over (or under) expression of these different myosin isoforms can have strong effects on actin organisation, cell shape, and contribute to the cancer phenotype as discussed in this review.

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Section: Myo9b and Myo18a Modulators Of Nm2 Filament Organisationmentioning

confidence: 99%

How myosin organization of the actin cytoskeleton contributes to the cancer phenotype

Peckham

2016

Biochemical Society Transactions

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“…Recently, we reported that acetylation of histones H3 and H4 surrounding the promoter region of the MYO18B gene correlates well with the level of MYO18B expression in lung cancer cells. 21 It was noted that TSA treatment led to upregulation of MYO18B expression in 2 cell lines, A2780 and SKOV3. This result strongly indicates that chromosomal condensation associated with histone deacetylation 22 also contributes to the silencing of the MYO18B gene in ovarian cancer cells, as in the case of lung cancer cells.…”

Section: Figure 2 -Expression Of the Myo18b Gene In Cancerous And Nonmentioning

confidence: 99%

Reduced expression of MYO18B, a candidate tumor‐suppressor gene on chromosome arm 22q, in ovarian cancer

Yanaihara

Nishioka²,

Kohno³

et al. 2004

Intl Journal of Cancer

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Allelic imbalance on chromosome arm 22q has been detected in 50 -70% of ovarian cancers, suggesting the presence of a tumor-suppressor gene on this chromosome arm that is involved in ovarian carcinogenesis. Recently, we isolated a candidate tumor-suppressor gene, MYO18B, at 22q12.1, which is deleted, mutated and hypermethylated in approximately 50% of lung cancers. In our study, we analyzed genetic and epigenetic alterations of the MYO18B gene in ovarian cancers. Missense MYO18B mutations were detected in 1 of 4 (25%) ovarian cancer cell lines and in 1 of 17 (5.9%) primary ovarian cancers. MYO18B expression was reduced in all 4 ovarian cancer cell lines and in 12 of 17 (71%) of primary ovarian cancers. MYO18B expression was restored by treatment with 5-aza-2-deoxycytidine and/or trichostatin A in 3 of 4 cell lines with reduced MYO18B expression, and hypermethylation of the promoter CpG island for MYO18B was observed in 2 of these 3 cell lines. Its hypermethylation was also observed in 2 of 15 (13%) primary ovarian cancers. Thus, it was indicated that MYO18B expression is reduced in a considerable fraction of ovarian cancers by several mechanisms, including hypermethylation, while the MYO18B gene is mutated in a small subset of ovarian cancers. The present results suggest that MYO18B alterations, including both epigenetic and genetic alterations, play an important role in ovarian carcinogenesis. © 2004 Wiley-Liss, Inc. Key words: tumor-suppressor gene; ovarian cancer; 22qOvarian cancer is the leading cause of death from gynecologic malignancies due to its aggressive nature and the fact that the majority of patients are diagnosed in advanced stages of the disease. To date, several types of genetic studies have been performed to understand the molecular pathways of ovarian carcinogenesis. [1][2][3][4][5] Approximately 5-10% of ovarian cancers are hereditary, and the remaining 90 -95% are sporadic. The majority of hereditary cancers occur in women with germline mutations of the BRCA1 or BRCA2 gene, whereas, in sporadic ovarian cancers, somatic mutations of the c-erbB-2, c-myc and K-ras oncogenes and of the p53 tumor-suppressor gene (TSG) have been frequently observed. However, genetic studies have further indicated that a number of other tumor-suppressor genes are also involved in ovarian carcinogenesis, since various chromosomal regions show high frequencies of allelic imbalance (AI) and, except for the p53 gene, there have been no known genes showing high frequencies of somatic mutations in ovarian cancers. Therefore, further efforts for the identification of target tumor-suppressor genes are needed to fully understand the molecular pathways of ovarian carcinogenesis.Deletions of chromosome arm 22q have been detected in 50 -70% of ovarian cancers by AI analyses. 6 -8 Deletions of chromosome 22 have also been observed by cytogenetic and comparative genomic hybridization analyses. 9 -11 Therefore, it has been indicated that chromosome arm 22q contains a TSG(s) playing a role in ovarian carcinogenesis. This chromosom...

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“…In addition to DNA methylation, histone hypoacetylation plays a critical role in epigenetic gene silencing (10). Chromatin inactivated by histone H3 and/or H4 deacetylation is associated with silencing of several cancer-related genes in cancer cells (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Genome-Wide Transcriptional Response to 5-Aza-2′-Deoxycytidine and Trichostatin A in Multiple Myeloma Cells

Heller¹,

Schmidt²,

Ziegler³

et al. 2008

Cancer Research

157

111

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To identify epigenetically silenced cancer-related genes and to determine molecular effects of 5-aza-2 ¶-deoxycytidine (AzadC) and/or trichostatin A (TSA) in multiple myeloma (MM), we analyzed global changes in gene expression profiles of three MM cell lines by microarray analysis. We identified up-regulation of several genes whose epigenetic silencing in MM is well known. However, much more importantly, we identified a large number of epigenetically inactivated cancerrelated genes that are involved in various physiologic processes and whose epigenetic regulation in MM was unknown thus far. In addition, drug treatment of MM cell lines resulted in down-regulation of several MM proliferationassociated factors (i.e., MAF, CCND1/2, MYC, FGFR3, MMSET). Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM. Methylation frequencies of these genes ranged between 0% and 17% in MGUS samples and between 5% and 50% in MM samples. Interestingly, methylation of SPARC and BNIP3 was statistically significantly associated with a poor overall survival of MM patients (P = 0.003 and P = 0.017, respectively). Moreover, SPARC methylation was associated with loss of SPARC protein expression by immunostaining in a subset of MM patients. In conclusion, we identified new targets for aberrant methylation in monoclonal gammopathies, and our results suggest that DNA methyltransferase and histone deacetylase inhibition might play an important role in the future treatment of patients with MM.

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Correlation between histone acetylation and expression of the MYO18B gene in human lung cancer cells

Cited by 32 publications

References 19 publications

How myosin organization of the actin cytoskeleton contributes to the cancer phenotype

How myosin organization of the actin cytoskeleton contributes to the cancer phenotype

Reduced expression of MYO18B, a candidate tumor‐suppressor gene on chromosome arm 22q, in ovarian cancer

Genome-Wide Transcriptional Response to 5-Aza-2′-Deoxycytidine and Trichostatin A in Multiple Myeloma Cells

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