Frequent and histological type-specific inactivation of 14-3-3σ in human lung cancers

Epigenetic silencing contributes to the loss of BRMS1 expression in breast cancer

“…Genes having significant relevance in breast cancer such as nm23, BRCA1, p16, and 14-3-3σ have been reported to also be under the control of epigenetic mechanisms suggesting that hypermethylation of genes is a broad spectrum phenomenon [31][32][33][34][35][36][37][38]. Methylation of 14-3-3σ is commonly seen in prostate cancer lesions, ovarian cancer, breast and lung carcinomas [34,[39][40][41][42][43][44]. The metastasis suppressor gene, nm23 is methylated in breast cancer and re-expression of the gene following treatment with 5-aza-2′-deoxycytidine resulted in a decrease in motility of the breast cancer cells [31].…”

Downregulation of 14-3-3σ in ovary, prostate and endometrial carcinomas is associated with CpG island methylation

“…Including our series, epigenetic transcriptional silencing of 14-3-3s has been demonstrated in malignancies from prostate, endometrium, ovary, breast, lung, liver, skin, stomach and oral squamous cell carcinoma. [15][16][17][18]20,21,[24][25][26] Another recent immunohistochemical study has shown loss of 14-3-3s expression in prostate cancer. 27 By preselecting areas of highest Gleason score in their tumor biopsies and by using a different 14-3-3s antibody, these authors find low or absent levels of 14-3-3s in an even higher percentage of tumors.…”

“…Following studies demonstrated epigenetic silencing of 14-3-3s expression in gastric, liver, lung, cervical, oral squamous cell carcinoma, and basal cell carcinoma of the skin. [16][17][18][19][20][21] The aims of this study were: first, to study the expression of 14-3-3s by using immunohistochemistry on a multiple tumor tissue microarrays containing a large number of urological and gynecological cancers. Second, to explore the relation between 14-3-3s expression and p53 using the D07 and the PAB240 clone recognizing wild-type and mutated p53 isoforms respectively.…”

Frequent downregulation of 14-3-3 σ protein and hypermethylation of 14-3-3 σ gene in salivary gland adenoid cystic carcinoma

“…subsequent step on the salivary gland carcinogenesis. Osada et al (2002) demonstrated that small-cell lung cancer cell lines frequently showed DNA hypermethylation of 14-3-3 s, but nonsmall-cell lung cancer cell lines did not. In our experiment, methylation pattern was quite different in the histological subtypes of SGCs, ACC, and MEC.…”

“…Moreover, Chan et al (1999) reported that 14-3-3 s-deficient cells were rapidly killed by ionizing radiation through a process known as mitotic catastrophe, which was associated with a failure of the cells to sequester cyclin B/CDC2 complex from the nucleus. More recently, it was shown that the expression of 14-3-3 s was frequently lost in several types of cancers due to hypermethylation of the gene (Ferguson et al, 2000;Iwata et al, 2000;Suzuki et al, 2000;Gasco et al, 2002a, b;Osada et al, 2002). These findings indicate that 14-3-3 s plays diverse roles not only in the radiosensitivity of the cells but also in tumorigenesis of several cancer, including SGCs.…”