Transgelin gene is frequently downregulated by promoter DNA hypermethylation in breast cancer

Sayar, Nilüfer; Karahan, Gurbet; Konu, Özlen; Bozkurt, Birkan; Bozdoğan, Önder; Yuluğ, Işık G.

doi:10.1186/s13148-015-0138-5

Cited by 36 publications

(27 citation statements)

References 84 publications

(97 reference statements)

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“…The detection of TAGLN expression in BT 549 and PMC 42 cells is in agreement with its expression in TNBC tumors and other TNBC cell lines [ 16,33 ] and in the immortalized normal epithelial breast cell lines, MCF10A and MCF12A. [ 13 ] We confirmed the association of TAGLN with the actin cytoskeleton in both cell lines. However, our results suggested that TAGLN silencing influenced different cellular processes in BT 549 and PMC 42 cells.…”

Section: Discussionsupporting

confidence: 83%

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Transgelin Silencing Induces Different Processes in Different Breast Cancer Cell Lines

et al. 2020

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Transgelin is a protein reported to be a marker of several cancers. However, previous studies have shown both up‐ and down‐regulation of transgelin in tumors when compared with non‐tumor tissues and the mechanisms whereby transgelin may affect the development of cancer remain largely unknown. Transgelin is especially abundant in smooth muscle cells and is associated with actin stress fibers. These contractile structures participate in cell motility, adhesion, and the maintenance of cell morphology. Here, the role of transgelin in breast cancer is focused on. Initially, the effects of transgelin on cell migration of the breast cancer cell lines, BT 549 and PMC 42, is studied. Interestingly, transgelin silencing increased the migration of PMC 42 cells, but decreased the migration of BT 549 cells. To clarify these contradictory results, the changes in protein abundances after transgelin silencing in these two cell lines are analyzed using quantitative proteomics. The results confirmed the role of transgelin in the migration of BT 549 cells and suggest the involvement of transgelin in apoptosis and small molecule biochemistry in PMC 42 cells. The context‐dependent function of transgelin reflects the different molecular backgrounds of these cell lines, which differ in karyotypes, mutation statuses, and proteome profiles.

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Section: Discussionsupporting

confidence: 83%

“…[ 12 ] Sayar et al. [ 13 ] tested 13 breast cancer cell lines for TAGLN protein levels by immunoblotting (with a polyclonal antibody) and found nine TAGLN‐positive cell lines with different TAGLN expression levels. The role of TAGLN has been studied in MCF7, MDA MB 231, and Hs578T cells.…”

Section: Introductionmentioning

confidence: 99%

Transgelin Silencing Induces Different Processes in Different Breast Cancer Cell Lines

et al. 2020

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“…SIDT2-deficient mice have increased serum triglyceride [ 32 ]. TAGLN (Transgelin, sm22α) is an actin-binding protein expressed in smooth muscle cells [ 33 ]. Yang et al [ 34 ] revealed that the most enriched pathways caused by SM22α knockout in mice were lipid metabolism, inflammation, and hematopoiesis.…”

Section: Discussionmentioning

confidence: 99%

Multiple genotype–phenotype association study reveals intronic variant pair on SIDT2 associated with metabolic syndrome in a Korean population

et al. 2018

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BackgroundMetabolic syndrome is a risk factor for type 2 diabetes and cardiovascular disease. We identified common genetic variants that alter the risk for metabolic syndrome in the Korean population. To isolate these variants, we conducted a multiple-genotype and multiple-phenotype genome-wide association analysis using the family-based quasi-likelihood score (MFQLS) test. For this analysis, we used 7211 and 2838 genotyped study subjects for discovery and replication, respectively. We also performed a multiple-genotype and multiple-phenotype analysis of a gene-based single-nucleotide polymorphism (SNP) set.ResultsWe found an association between metabolic syndrome and an intronic SNP pair, rs7107152 and rs1242229, in SIDT2 gene at 11q23.3. Both SNPs correlate with the expression of SIDT2 and TAGLN, whose products promote insulin secretion and lipid metabolism, respectively. This SNP pair showed statistical significance at the replication stage.ConclusionsOur findings provide insight into an underlying mechanism that contributes to metabolic syndrome.Electronic supplementary materialThe online version of this article (10.1186/s40246-018-0180-4) contains supplementary material, which is available to authorized users.

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“…Previous studies have demonstrated that SM22α may be involved in the development and progression of malignant tumors. Decreased expression of SM22α has been reported in lung, prostate, renal and breast cancer ( 17 – 20 ). Zhang et al ( 21 ) reported that SM22α may induce apoptosis via interacting with p53 in prostate cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence suggests that SM22α may act as a tumor suppressor. Previous studies reported decreased expression of SM22α in several types of human cancer, including lung, prostate, renal and breast cancer ( 17 – 20 ). The function of SM22α was also reported to be associated with increased apoptosis of prostate cancer cells ( 21 ).…”

Section: Introductionmentioning

confidence: 96%

Downregulation of SM22α protein by hypermethylation of its promoter in colorectal cancer

et al. 2018

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Silencing of tumor suppressor genes by hypermethylation in gene promoter regions is a crucial mechanism in carcinogenesis. Gene methylation may be reversible and evaluated easily, thus providing a promising substrate for the development of biomarkers for the detection and prevention of cancer, including colorectal cancer (CRC). In the present study, the protein expression and methylation status of smooth muscle protein 22α (SM22α) was investigated in 78 cases of CRC and adjacent normal tissue. The aim of the study was to investigate the function of SM22α in the pathogenesis of CRC and to identify a candidate biomarker for the early detection of CRC. The methylation status of promoter of SM22α gene was detected using methylation-specific polymerase chain reaction. The protein expression of SM22α was evaluated using western blot analysis. The results demonstrated a significant decrease of SM22α protein expression in 50 (68.5%) cases of CRC compared with that in adjacent normal tissues (P<0.001). The methylation status of SM22α promoter in CRC was significantly increased compared with that in adjacent normal tissues (P<0.001). Additionally, there was a negative correlation between the expression of SM22α protein and methylation levels of SM22α gene in CRC (P<0.001). Kaplan-Meier curves revealed that patients with CRC with an unmethylated promoter of SM22α gene exhibited an increased survival time (34.8±0.6 vs. 30.9±1.3 months; P=0.025) compared with that in patients with a methylated promoter of SM22α gene. The present study demonstrated that the protein expression of SM22α is downregulated in CRC tissues by hypermethylation of its promoter, and that the methylation of SM22 α promoter may be used as a biomarker for early detection, prognosis and prediction of CRC.

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Transgelin gene is frequently downregulated by promoter DNA hypermethylation in breast cancer

Cited by 36 publications

References 84 publications

Transgelin Silencing Induces Different Processes in Different Breast Cancer Cell Lines

Transgelin Silencing Induces Different Processes in Different Breast Cancer Cell Lines

Multiple genotype–phenotype association study reveals intronic variant pair on SIDT2 associated with metabolic syndrome in a Korean population

Downregulation of SM22α protein by hypermethylation of its promoter in colorectal cancer

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